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Arch Physiol Biochem. 2011, 117 (2): 47-56. 10.3109\u002F13813455.2010.535835.\nTrayhurn P, Wood IS: Adipokines: inflammation and the pleiotropic role of white adipose tissue. Br J Nutr. 2004, 92 (3): 347-355. 10.1079\u002FBJN20041213.\nde Heredia FP, Sonia G-M, Ascension M: Chronic and degenerative diseases: obesity, inflammation and the immune system. Proc Nutr Soc. 2012, 71: 332-338. 10.1017\u002FS0029665112000092.\nStraub RH, Cutolo M, Zietz B, Scholmerich J: The process of aging changes the interplay of the immune, endocrine and nervous systems. Mech Ageing Dev. 2001, 122 (14): 1591-1611. 10.1016\u002FS0047-6374(01)00289-5.\nPhillips AC, Carroll D, Gale CR, Lord JM, Arlt W, Batty GD: Cortisol, DHEA sulphate, their ratio, and all-cause and cause-specific mortality in the Vietnam Experience Study. Eur J Endocrinol. 2010, 163 (2): 285-292. 10.1530\u002FEJE-10-0299.\nTurnbull AV, Rivier CL: Regulation of the hypothalamic-pituitary-adrenal axis by cytokines: actions and mechanisms of action. Physiol Rev. 1999, 79 (1): 1-71.\nStraub RH, Miller LE, Scholmerich J, Zietz B: Cytokines and hormones as possible links between endocrinosenescence and immunosenescence. J Neuroimmunol. 2000, 109 (1): 10-15. 10.1016\u002FS0165-5728(00)00296-4.\nSergio G: Exploring the complex relations between inflammation and aging (inflamm-aging): anti-inflamm-aging remodelling of inflamm-aging, from robustness to frailty. Inflamm Res. 2008, 57 (12): 558-563. 10.1007\u002Fs00011-008-7243-2.\nRosenfeld RS, Rosenberg BJ, Fukushima DK, Hellman L: 24-hour secretory pattern of dehydroisoandrosterone and dehydroisoandrosterone sulfate. J Clin Endocrinol Metab. 1975, 40 (5): 850-855. 10.1210\u002Fjcem-40-5-850.\nLabrie F: DHEA, important source of sex steroids in men and even more in women. Prog Brain Res. 2010, 182: 97-148.\nButcher SK, Killampalli V, Lascelles D, Wang K, Alpar EK, Lord JM: Raised cortisol:DHEAS ratios in the elderly after injury: potential impact upon neutrophil function and immunity. Aging Cell. 2005, 4 (6): 319-324. 10.1111\u002Fj.1474-9726.2005.00178.x.\nArlt W, Hammer F, Sanning P, Butcher SK, Lord JM, Allolio B, Annane D, Stewart PM: Dissociation of serum dehydroepiandrosterone and dehydroepiandrosterone sulfate in septic shock. J Clin Endocrinol Metab. 2006, 91 (7): 2548-2554. 10.1210\u002Fjc.2005-2258.\nPhillips AC, Carroll D, Gale CR, Lord JM, Arlt W, Batty GD: Cortisol, DHEAS, their ratio and the metabolic syndrome: evidence from the Vietnam experience study. Eur J Endocrinol. 2010, 162 (5): 919-923. 10.1530\u002FEJE-09-1078.\nPetri MA, Mease PJ, Merrill JT, Lahita RG, Iannini MJ, Yocum DE, Ginzler EM, Katz RS, Gluck OS, Genovese MC, Van Vollenhoven R, Kalunian KC, Manzi S, Greenwald MW, Buyon JP, Olsen NJ, Schiff MH, Kavanaugh AF, Caldwell JR, Ramsey-Goldman R, St Clair EW, Goldman AL, Egan RM, Polisson RP, Moder KG, Rothfield NF, Spencer RT, Hobbs K, Fessler BJ, Calabrese LH: Effects of prasterone on disease activity and symptoms in women with active systemic lupus erythematosus. Arthritis Rheum. 2004, 50 (9): 2858-2868. 10.1002\u002Fart.20427.\nChang DM, Lan JL, Lin HY, Luo SF: Dehydroepiandrosterone treatment of women with mild-to-moderate systemic lupus erythematosus: a multicenter randomized, double-blind, placebo-controlled trial. Arthritis Rheum. 2002, 46 (11): 2924-2927. 10.1002\u002Fart.10615.\nSawalha AH, Kovats S: Dehydroepiandrosterone in systemic lupus erythematosus. Curr Rheumatol Rep. 2008, 10 (4): 286-291. 10.1007\u002Fs11926-008-0046-1.\nBaylis D, Bartlett DB, Syddall HE, Ntani G, Gale CR, Cooper C, Lord JM, Sayer AA: Immune-endocrine biomarkers as predictors of frailty and mortality: a 10-year longitudinal study in community-dwelling older people. Age (Dordr). 2012, 10.1007\u002Fs11357-012-9396-8.\nGao HM, Hong JS: Why neurodegenerative diseases are progressive: uncontrolled inflammation drives disease progression. Trends Immunol. 2008, 29 (8): 357-365. 10.1016\u002Fj.it.2008.05.002.\nLibby P: Inflammation in atherosclerosis. Arterioscler Thromb Vasc Biol. 2012, 32 (9): 2045-2051. 10.1161\u002FATVBAHA.108.179705.\nGiunta B, Fernandez F, Nikolic WV, Obregon D, Rrapo E, Town T, Tan J: Inflammaging as a prodrome to Alzheimer’s disease. J Neuroinflammation. 2008, 5: 51-10.1186\u002F1742-2094-5-51.\nSaini A, Faulkner S, Al-Shanti N, Stewart C: Powerful signals for weak muscles. Ageing Res Rev. 2009, 8 (4): 251-267. 10.1016\u002Fj.arr.2009.02.001.\nCesari M, Penninx BW, Pahor M, Lauretani F, Corsi AM, Rhys Williams G, Guralnik JM, Ferrucci : Inflammatory markers and physical performance in older persons: the InCHIANTI study. J Gerontol A Biol Sci Med Sci. 2004, 59 (3): 242-248. 10.1093\u002Fgerona\u002F59.3.M242.\nSchaap LA, Pluijm SM, Deeg DJ, Harris TB, Kritchevsky SB, Newman AB, Colbert LH, Pahor M, Rubin SM, Tylavsky FA, Visser M, Health ABC Study: Higher inflammatory marker levels in older persons: associations with 5-year change in muscle mass and muscle strength. J Gerontol A Biol Sci Med Sci. 2009, 64 (11): 1183-1189.\nPayette H, Roubenoff R, Jacques PF, Dinarello CA, Wilson PW, Abad LW, Harris T: Insulin-like growth factor-1 and interleukin 6 predict sarcopenia in very old community-living men and women: the Framingham heart study. J Am Geriatr Soc. 2003, 51 (9): 1237-1243. 10.1046\u002Fj.1532-5415.2003.51407.x.\nRohleder N, Kudielka BM, Hellhammer DH, Wolf JM, Kirschbaum C: Age and sex steroid-related changes in glucocorticoid sensitivity of pro-inflammatory cytokine production after psychosocial stress. J Neuroimmunol. 2002, 126 (1–2): 69-77.\nBeyer I, Mets T, Bautmans I: Chronic low-grade inflammation and age-related sarcopenia. Curr Opin Clin Nutr Metab Care. 2012, 15 (1): 12-22. 10.1097\u002FMCO.0b013e32834dd297.\nLencel P, Magne D: Inflammaging: the driving force in osteoporosis?. Med Hypotheses. 2011, 76 (3): 317-321. 10.1016\u002Fj.mehy.2010.09.023.\nChristensen H, Boysen G, Johannesen HH: Serum-cortisol reflects severity and mortality in acute stroke. J Neurol Sci. 2004, 217 (2): 175-180. 10.1016\u002Fj.jns.2003.09.013.\nSam S, Corbridge TC, Mokhlesi B, Comellas AP, Molitch ME: Cortisol levels and mortality in severe sepsis. Clin Endocrinol (Oxf). 2004, 60 (1): 29-35. 10.1111\u002Fj.1365-2265.2004.01923.x.\nGüder G, Bauersachs J, Frantz S, Weismann D, Allolio B, Ertl G, Angermann CE, Störk S: Complementary and incremental mortality risk prediction by cortisol and aldosterone in chronic heart failure. Circulation. 2007, 115 (13): 1754-1761. 10.1161\u002FCIRCULATIONAHA.106.653964.\nWaters DL, Qualls CR, Dorin RI, Veldhuis JD, Baumgartner RN: Altered growth hormone, cortisol, and leptin secretion in healthy elderly persons with sarcopenia and mixed body composition phenotypes. J Gerontol A Biol Sci Med Sci. 2008, 63 (5): 536-541. 10.1093\u002Fgerona\u002F63.5.536.\nStraub RH, Lehle K, Herfarth H, Weber M, Falk W, Preuner J, Scholmerich J: Dehydroepiandrosterone in relation to other adrenal hormones during an acute inflammatory stressful disease state compared with chronic inflammatory disease: role of interleukin-6 and tumour necrosis factor. Eur J Endocrinol. 2002, 146 (3): 365-374. 10.1530\u002Feje.0.1460365.\nTrivedi DP, Khaw KT: Dehydroepiandrosterone sulfate and mortality in elderly men and women. J Clin Endocrinol Metab. 2001, 86 (9): 4171-4177. 10.1210\u002Fjc.86.9.4171.\nMazat L, Lafont S, Berr C, Debuire B, Tessier JF, Dartigues JF, Baulieu EE: Prospective measurements of dehydroepiandrosterone sulfate in a cohort of elderly subjects: relationship to gender, subjective health, smoking habits, and 10-year mortality. Proc Natl Acad Sci USA. 2001, 98 (14): 8145-8150. 10.1073\u002Fpnas.121177998.\nValenti G, Denti L, Maggio M, Ceda G, Volpato S, Bandinelli S, Ceresini G, Cappola A, Guralnik JM, Ferrucci L: Effect of DHEAS on skeletal muscle over the life span: the InCHIANTI study. J Gerontol A Biol Sci Med Sci. 2004, 59 (5): 466-472. 10.1093\u002Fgerona\u002F59.5.M466.",{"EN":498},"Inflammaging is characterized by the upregulation of the inflammatory response that occurs with advancing age; its roots are strongly embedded in evolutionary theory. Inflammaging is believed to be a consequence of a remodelling of the innate and acquired immune system, resulting in chronic inflammatory cytokine production. Complex interrelated genetic, environmental and age-related factors determine an individual’s vulnerability or resilience to inflammaging. These factors include polymorphisms to the promoter regions of cytokines, cytokine receptors and antagonists, age-related decreases in autophagy and increased adiposity. Anti-inflammaging describes the upregulation of the hypothalamic-pituitary axis in response to inflammaging, leading to higher levels of cortisol, which in turn may be detrimental, contributing to less successful ageing and frailty. This may be countered by the adrenal steroid dehydroepiandrosterone, which itself declines with age, leaving certain individuals more vulnerable. Inflammaging and anti-inflammaging have both been linked with a number of age-related outcomes, including chronic morbidity, functional decline and mortality. This important area of research offers unique insights into the ageing process and the potential for screening and targeted interventions.",{"EN":500},"Understanding how we age: insights into inflammaging",{"VOID":502},"10.1186\u002F2046-2395-2-8","https:\u002F\u002Flongevityandhealthspan.biomedcentral.com\u002Farticles\u002F10.1186\u002F2046-2395-2-8",[505,533,552,571],{"id":506,"sortIndex":19,"researcher":18,"roles":507,"affiliations":509,"properties":530},"8908a1d2-be5c-4724-be52-e49641477f46",[508],"AUTHOR",[510,522],{"id":511,"sortIndex":102,"affiliation":512,"properties":521},"bbb66153-344b-41f2-b564-73dc9c6a3397",{"id":513,"createTime":514,"updateTime":515,"relativeEntities":516,"slug":517,"properties":518,"entityType":92,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"20e3899b-0a21-41b4-af8d-83ee07a5f27f","2024-04-18T23:58:46.752+00:00","2024-12-22T19:48:31.520+00:00",[],"Academic-Geriatric-Medicine-University-of-Southampton-Southampton-UK",{"title":519},{"EN":520},"Academic Geriatric Medicine, University of Southampton, Southampton, UK",{},{"id":18,"sortIndex":19,"affiliation":523,"properties":18},{"id":524,"createTime":525,"updateTime":525,"relativeEntities":526,"slug":18,"properties":527,"entityType":92,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"19916cc9-bc8d-4748-85fd-1891fd4c7de9","2023-12-31T12:13:35.354+00:00",[],{"title":528},{"VI":529},"Department of Medicine for Older People, University Hospital Southampton, Southampton, UK",{"title":531},{"VI":532},"Daniel 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SV, Faulkner JA: Contractile properties of skeletal muscles from young, adult and aged mice. J Physiol (Lond). 1988, 404: 71-82.\nBaumgartner RN, Koehler KM, Gallagher D, Romero L, Heymsfield SB, Ross RR, Garry PJ, Lindeman RD: Epidemiology of sarcopenia among the elderly in New Mexico. Am J Epidemiol. 1998, 147: 755-763.\nBortz WM: A conceptual framework of frailty: a review. J Gerontol A Biol Sci Med Sci. 2002, 57: M283-M288.\nCesari M, Leeuwenburgh C, Lauretani F, Onder G, Bandinelli S, Maraldi C, Guralnik JM, Pahor M, Ferrucci L: Frailty syndrome and skeletal muscle: results from the Invecchiare in Chianti study. Am J Clin Nutr. 2006, 83: 1142-1148.\nClaflin DR, Larkin LM, Cederna PS, Horowitz JF, Alexander NB, Cole NM, Galecki AT, Chen S, Nyquist LV, Carlson BM, Faulkner JA, Ashton-Miller JA: Effects of high- and low-velocity resistance training on the contractile properties of skeletal muscle fibers from young and older humans. J Appl Physiol. 2011, 111: 1021-1030.\nCohen HJ: In search of the underlying mechanisms of frailty. J Gerontol. 2000, 55: M706-M708.\nEspinoza S, Walston JD: Frailty in older adults: insights and interventions. Cleve Clin J Med. 2005, 72: 1105-1112.\nFried LP: Conference on the physiologic basis of frailty. Aging (Milano). 1992, 4: 251-265.\nFried LP, Tangen CM, Walston J, Newman AB, Hirsch C, Gottdiener J, Seeman T, Tracy R, Kop WJ, Burke G, McBurnie MA, Cardiovascular Health Study Collaborative Research Group: Frailty in older adults: evidence for a phenotype. J Gerontol A Biol Sci Med Sci. 2001, 56: M146-M156.\nFrontera WR, Hughes VA, Fielding RA, Fiatarone MA, Evans WJ, Roubenoff R: Aging of skeletal muscle: a 12-yr longitudinal study. J Appl Physiol. 2000, 88: 1321-1326.\nFrontera WR, Reid KF, Phillips EM, Krivickas LS, Hughes VA, Roubenoff R, Fielding RA: Muscle fiber size and function in elderly humans: a longitudinal study. J Appl Physiol. 2008, 105: 637-642.\nHadley EC, Ory MG, Suzman R, Weindruch R, Fried L: Physical frailty: a treatable cause of dependence in old age. J Gerontol. 1993, 48: 1-88.\nHamerman D: Toward an understanding of frailty. Ann Intern Med. 1999, 130: 945-950.\nHepple RT: Muscle atrophy is not always sarcopenia. J Appl Physiol. 2012, Epub ahead of print\nJanssen I: Influence of sarcopenia on the development of physical disability: the Cardiovascular Health Study. J Am Geriatr Soc. 2006, 54: 56-62.\nLexell J, Downham D, Sjostrom M: Distribution of different fibre types in human skeletal muscles. Fibre type arrangement in m. vastus lateralis from three groups of healthy men between 15 and 83 years. J Neurol Sci. 1986, 72: 211-222.\nLexell J, Taylor CC, Sjostrom M: What is the cause of the ageing atrophy? Total number, size and proportion of different fiber types studied in whole vastus lateralis muscle from 15- to 83-year-old men. J Neurol Sci. 1988, 84: 275-94.\nLord SR, Sherrington C, Menz HB: Falls in Older People. Risk Factors and Strategies for Prevention. 2001, Cambridge: Cambridge University Press,\nSchultz AB: Muscle function and mobility biomechanics in the elderly: an overview of some recent research. J Gerontol. 1995, 50A: 60-63.\nTinetti ME, Williams TF, Mayewski R: Fall risk index for elderly patients based on number of chronic disabilities. Am J Med. 1986, 80: 429-434.\nYoung A, Skelton DA: Applied physiology of strength and power in old age. Int J Sports Med. 1994, 15: 149-151.\nPearson SJ, Young A, Macaluso A, Devito G, Nimmo MA, Cobbold M, Harridge SD: Muscle function in elite master weightlifters. Med Sci Sports Exerc. 2002, 34: 1199-1206.\nIWF: Masters Records – Men, July 18. 2012, http:\u002F\u002Fwww.iwfmasters.net\u002Frecords\u002Fiwf-men.pdf, . Age Group 35 – 39, M35,\nJones A: Age grading running races. http:\u002F\u002Fhome.roadrunner.com\u002F~alanjones\u002FAgeGrade.html,\nBalice-Gordon R: Age-related changes in neuromuscular innervation. Muscle Nerve Suppl . 1997, 5: S83-S87.\nCourtney J, Steinbach JH: Age changes in neuromuscular junction morphology and acetylcholine receptor distribution on rat skeletal muscle fibres. J. Physiol. 1981, 320: 435-447.\nDeschenes MR: Motor unit and neuromuscular junction remodeling with aging. Curr Aging Sci. 2011, 4: 209-220.\nJang YC, Van Remmen H: Age-associated alterations of the neuromuscular junction. Exp Gerontol. 2011, 46: 193-198.\nLuff AR: Age-associated changes in the innervation of muscle fibers and changes in the mechanical properties of motor units. Ann N Y Acad Sci. 1998, 854: 92-101.\nValdez G, Tapia JC, Kang H, Clemenson GDJ, Gage FH, Lichtman JW, Sanes JR: Attenuation of age-related changes in mouse neuromuscular synapses by caloric restriction and exercise. Proc Natl Acad Sci U S A. 2010, 107: 14863-14868.\nGopinath SD, Rando TA: Stem cell review series: aging of the skeletal muscle stem cell niche. Aging Cell. 2008, 7: 590-598.\nGeorge T, Velloso CP, Alsharidah M, Lazarus NR, Harridge SD: Sera from young and older humans equally sustain proliferation and differentiation of human myoblasts. Exp Gerontol. 2010, 45: 875-881.\nJackson MJ, McArdle A: Age-related changes in skeletal muscle reactive oxygen species generation and adaptive responses to reactive oxygen species. J Physiol. 2011, 589: 2139-2145.\nAltun M, Besche HC, Overkleeft HS, Piccirillo R, Edelmann MJ, Kessler BM, Goldberg AL, Ulfhake B: Muscle wasting in aged, sarcopenic rats is associated with enhanced activity of the ubiquitin proteasome pathway. J Biol Chem. 2010, 285: 39597-39608.\nRennie MJ, Selby A, Atherton P, Smith K, Kumar V, Glover EL, Philips SM: Facts, noise and wishful thinking: muscle protein turnover in aging and human disuse atrophy. Scand J Med Sci Sports. 2010, 20: 5-9.\nHuang JH, Hood DA: Age-associated mitochondrial dysfunction in skeletal muscle: Contributing factors and suggestions for long-term interventions. IUBMB Life. 2009, 61: 201-214.\nJang YC, Lustgarten MS, Liu Y, Muller FL, Bhattacharya A, Liang H, Salmon AB, Brooks SV, Larkin L, Hayworth CR, Richardson A, Van Remmen H: Increased superoxide in vivo accelerates age-associated muscle atrophy through mitochondrial dysfunction and neuromuscular junction degeneration.FASEB J. 2010, 24: 1376-1390.\nMuller FL, Song W, Jang YC, Liu Y, Sabia M, Richardson A, Van Remmen H: Denervation-induced skeletal muscle atrophy is associated with increased mitochondrial ROS production. Am J Physiol Regul Integr Comp Physiol. 2007, 293: R1159-R1168.\nDegens H: The role of systemic inflammation in age-related muscle weakness and wasting. Scand J Med Sci Sports. 2010, 20: 28-38.\nReid MB, Moylan JS: Beyond atrophy: redox mechanisms of muscle dysfunction in chronic inflammatory disease. J Physiol. 2011, 589: 2171-2179.",{"EN":617},"An international workshop was hosted by the University of Liverpool on 15–16 July 2011 to address at a basic level what is known about the fundamental mechanisms by which skeletal muscle mass and function are lost during aging and to examine the nature of interventions that might prevent these mechanistic changes. Of particular importance was to attempt to evaluate how different forms of exercise (or muscle contractile activity) influence these processes and how these effects can be best optimized to prevent or delay age-related loss of muscle function. The program took the form of a two-day meeting, comprising a series of invited talks and breakout sessions designed to identify key gaps in current knowledge and potential future research questions. The aims of this Workshop were two-fold: 1. To identify the current state-of-the-art in the understanding of the mechanisms that contribute to loss of skeletal muscle mass and function that occurs with aging and to address at a mechanistic level how, and to what extent, exercise and\u002For other interventions might prevent these changes. 2. To identify specific areas of research where information is sparse but which are likely to yield data that will impact on future strategies to manipulate age-related loss of muscle mass and function in older people. The areas discussed in detail were loss of functional motor units, reduced muscle stem cell activity, age-related changes in transcriptional responses of muscle to exercise and nutrition, age-related changes in protein homeostasis, mitochondrial function, altered cross-talk between muscle with immune cells and how the developments in basic science to understand mechanisms underlying age-related loss of muscle mass and function can be translated. Following each session three key areas where further studies are needed were identified.",{"EN":619},"Workshop report: Can an understanding of the mechanisms underlying age-related loss of muscle mass and function guide exercise and other intervention strategies?",{"VOID":621},"10.1186\u002F2046-2395-1-5","https:\u002F\u002Flongevityandhealthspan.biomedcentral.com\u002Farticles\u002F10.1186\u002F2046-2395-1-5",[624,641,653,665],{"id":625,"sortIndex":79,"researcher":18,"roles":626,"affiliations":627,"properties":638},"9d9701c4-45fe-4835-b663-a41e8738a01c",[508],[628],{"id":18,"sortIndex":19,"affiliation":629,"properties":18},{"id":630,"createTime":631,"updateTime":632,"relativeEntities":633,"slug":634,"properties":635,"entityType":92,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"024724a9-c6b7-4df0-861e-faeb6cf19fb9","2024-02-06T08:38:54.948+00:00","2025-06-11T15:41:47.773+00:00",[],"Institute-of-Ageing-and-Chronic-Disease-University-of-Liverpool-Liverpool-UK",{"title":636},{"VI":637},"Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool, UK",{"title":639},{"VI":640},"Aphrodite Vasilaki",{"id":642,"sortIndex":29,"researcher":18,"roles":643,"affiliations":644,"properties":650},"0f594c9d-2bed-458b-a964-8643e991bdb3",[508],[645],{"id":18,"sortIndex":19,"affiliation":646,"properties":18},{"id":630,"createTime":631,"updateTime":632,"relativeEntities":647,"slug":634,"properties":648,"entityType":92,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":649},{"VI":637},{"title":651},{"VI":652},"Anna Kayani",{"id":654,"sortIndex":102,"researcher":18,"roles":655,"affiliations":656,"properties":662},"f5183cd4-cbc8-4ae4-a148-89686dfe89e9",[508],[657],{"id":18,"sortIndex":19,"affiliation":658,"properties":18},{"id":630,"createTime":631,"updateTime":632,"relativeEntities":659,"slug":634,"properties":660,"entityType":92,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":661},{"VI":637},{"title":663},{"VI":664},"Anne McArdle",{"id":666,"sortIndex":19,"researcher":18,"roles":667,"affiliations":668,"properties":674},"711ec031-842c-4bc3-99b7-e42b10773b76",[508],[669],{"id":18,"sortIndex":19,"affiliation":670,"properties":18},{"id":630,"createTime":631,"updateTime":632,"relativeEntities":671,"slug":634,"properties":672,"entityType":92,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":673},{"VI":637},{"title":675},{"VI":676},"Malcolm J Jackson",{"url":622,"publisher":678,"properties":691},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":679,"slug":10,"properties":680,"entityType":16,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"subjectFields":683,"manageAffiliations":684,"indexDatabases":685,"url":18,"thumbnailPath":18,"statistic":686,"gsStatistic":18,"type":18,"analyzePriority":18},[],{"eissn":681,"title":682},{"VOID":13},{"EN":15},[],[],[],{"impactFactor":19,"impactFactorByYear":687,"i10Index":29,"i10IndexLast5Year":19,"totalPublication":30,"totalPublicationByYear":688,"totalCitation":35,"totalCitationByYear":689,"totalCitationPerPublication":40,"totalCitationPerPublicationByYear":690,"hindexLast5Year":29,"hindex":29},{"2013":25,"2014":26,"2015":27,"2016":28},{"2012":32,"2013":33,"2014":34},{"2012":37,"2013":38,"2014":39},{"2012":42,"2013":43,"2014":44},{"volume":692,"pages":694},{"VOID":693},"1",{"VOID":695},"1-5","2012-10-01",2012,{"id":699,"createTime":700,"updateTime":700,"relativeEntities":701,"slug":702,"properties":703,"entityType":70,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"primaryUrl":710,"fullTextUrl":18,"authors":711,"publicationType":136,"publisherRelationship":775,"citationCount":18,"citationInfo":18,"publishDate":793,"publishYear":606,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":18,"openAccess":18,"references":18,"isForceReanalyzing":487},"e9735c51-1600-43fc-bf45-059ef746bc49","2023-11-27T21:47:39.052+00:00",[],"Erratum-to-Lifespan-extension-and-delay-of-age-related-functional-decline-caused-by-Rhodiola-roseadepends-on-dietary-macronutrient-balance",{"references":704,"title":706,"doi":708},{"VOID":705},"Gospodaryov , et al: Lifespan extension and delay of age-related functional decline caused by Rhodiola rosea depends on dietary macronutrient balance. Longevity & Healthspan. 2013, 2: 5-10.1186\u002F2046-2395-2-5.",{"EN":707},"Erratum to: Lifespan extension and delay of age-related functional decline caused by Rhodiola roseadepends on dietary macronutrient balance",{"VOID":709},"10.1186\u002F2046-2395-2-12","https:\u002F\u002Flongevityandhealthspan.biomedcentral.com\u002Farticles\u002F10.1186\u002F2046-2395-2-12",[712,727,751,763],{"id":713,"sortIndex":29,"researcher":18,"roles":714,"affiliations":715,"properties":724},"4863127c-adda-4772-b20f-fe8d9f24c800",[508],[716],{"id":18,"sortIndex":19,"affiliation":717,"properties":18},{"id":718,"createTime":719,"updateTime":719,"relativeEntities":720,"slug":18,"properties":721,"entityType":92,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"8f0d26de-7329-4b13-a37e-e2bf11d55437","2024-02-17T02:23:33.605+00:00",[],{"title":722},{"VI":723},"Department of Biochemistry and Biotechnology, Vassyl Stefanyk Precarpathian 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D: Aging: a theory based on free radical and radiation chemistry. J Gerontol. 1956, 11: 298-300. 10.1093\u002Fgeronj\u002F11.3.298.\nHarman D: The biologic clock: the mitochondria?. J Am Geriat Soc. 1972, 20: 145-147.\nHarman D: The aging process. Proc Natl Acad Sci U S A. 1981, 78: 7124-7128. 10.1073\u002Fpnas.78.11.7124.\nAmaral S, Amaral A, Ramalho-Santos J: Aging and male reproductive function: a mitochondrial perspective. Front Biosci (Schol Ed). 2013, 5: 181-197.\nHauser DN, Hastings TG: Mitochondrial dysfunction and oxidative stress in Parkinson’s disease and monogenic parkinsonism. Neurobiol Dis. 2013, 51: 35-42.\nJohnson ML, Robinson MM, Nair KS: Skeletal muscle aging and the mitochondrion. Trends Endocrinol Metab. 2013, 24: 247-256. 10.1016\u002Fj.tem.2012.12.003.\nVitale G, Salvioli S, Franceschi C: Oxidative stress and the ageing endocrine system. Nat Rev Endocrinol. 2013, 9: 228-240. 10.1038\u002Fnrendo.2013.29.\nMurphy MP: How mitochondria produce reactive oxygen species. Biochem J. 2009, 417: 1-13. 10.1042\u002FBJ20081386.\nSohal RS, Brunk UT: Mitochondrial production of pro-oxidants and cellular senescence. Mutat Res. 1992, 275: 295-304. 10.1016\u002F0921-8734(92)90033-L.\nJamieson D, Chance B, Cadenas E, Boveris A: The relation of free radical production to hyperoxia. Ann Rev Physiol. 1986, 48: 703-709. 10.1146\u002Fannurev.ph.48.030186.003415.\nTurrens JF, Freeman BA, Crapo JD: Hyperoxia increases H2O2 release by lung mitochondria and microsomes. Arch Biochem Biophys. 1982, 217: 411-421. 10.1016\u002F0003-9861(82)90519-7.\nLaw R, Bukwirwa H: The physiology of oxygen delivery. Update Anaesthesia. 1999, 10: 20-25.\nFelix MA, Braendle C: The natural history of Caenorhabditis elegans. Curr Biol. 2010, 20: R965-R969. 10.1016\u002Fj.cub.2010.09.050.\nHonda S, Ishii N, Suzuki K, Matsuo M: Oxygen dependent perturbation of lifespan and the aging rate in the nematode. J Gerontol. 1993, 48: B57-B61. 10.1093\u002Fgeronj\u002F48.2.B57.\nYanase S, Ishii N: Hyperoxia exposure induced hormesis decreases mitochondrial superoxide radical levels via Ins\u002FIGF-1 signaling pathway in a long-lived age-1 mutant of Caenorhabditis elegans. J Radiat Res. 2008, 49: 211-218. 10.1269\u002Fjrr.07043.\nDoonan R, McElwee JJ, Matthijssens F, Walker GA, Houthoofd K, Back P, Matscheski A, Vanfleteren JR, Gems D: Against the oxidative damage theory of aging: superoxide dismutases protect against oxidative stress but have little or no effect on lifespan in Caenorhabditis elegans. Genes Dev. 2008, 22: 3236-3241. 10.1101\u002Fgad.504808.\nVan Voorhies WA, Ward S: Broad oxygen tolerance in the nematode Caenorhabditis elegans. J Exp Biol. 2000, 203: 2467-2478.\nAnnefeld M, Erne B, Rasser Y: Ultrastructural analysis of rat articular cartilage following treatment with dexamethasone and glycosaminoglycan-peptide complex. Clin Exp Rheumatol. 1990, 8: 151-157.\nBarth E, Stämmler G, Speiser B, Schaper J: Ultrastructural quantitation of mitochondria and myofilaments in cardiac muscle from 10 different animal species including man. J Mol Cell Cardiol. 1992, 24: 669-681. 10.1016\u002F0022-2828(92)93381-S.\nFrederiks WM, Bosch KS: Localization of superoxide dismutase activity in rat tissues. Free Radic Biol Med. 1997, 22: 241-248. 10.1016\u002FS0891-5849(96)00328-0.\nHorvath S: DNA methylation age of human tissues and cell types. Genome Biol. 2013, 14: R115-10.1186\u002Fgb-2013-14-10-r115.\nRobb EL, Christoff CA, Maddalena LA, Stuart JA: Mitochondrial reactive oxygen species in animal cells: relevance to aging and normal physiology. Can J Zool. 2014,  :  -In press\nSanz A, Fernández-Ayala DJ, Stefanatos RK, Jacobs HT: Mitochondrial ROS production correlates with, but does not directly regulate lifespan in Drosophila. Aging (Albany NY). 2010, 2: 200-223.\nLabinskyy N, Csiszar A, Orosz Z, Smith K, Rivera A, Buffenstein R, Ungvari Z: Comparison of endothelial function, O2–* and H2O2 production, and vascular oxidative stress resistance between the longest-living rodent, the naked mole rat, and mice. Am J Physiol. 2006, 291: H2698-H2704.\nLambert AJ, Boysen HM, Buckingham JA, Yang T, Podlutsky A, Austad SN, Kunz TH, Buffenstein R, Brand MD: Low rates of hydrogen peroxide production by isolated heart mitochondria associate with long maximum lifespan in vertebrate homeotherms. Aging Cell. 2007, 6: 607-618. 10.1111\u002Fj.1474-9726.2007.00312.x.\nBrown JC, McClelland GB, Faure PA, Klaiman JM, Staples JF: Examining the mechanisms responsible for lower ROS release rates in liver mitochondria from the long-lived house sparrow (Passer domesticus) and big brown bat (Eptesicus fuscus) compared to the short-lived mouse (Mus musculus). 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Free Radic Biol Med. 2014, 66: 88-99.\nSmith RA, Hartley RC, Cochemé HM, Murphy MP: Mitochondrial pharmacology. Trends Pharmacol Sci. 2012, 33: 341-352. 10.1016\u002Fj.tips.2012.03.010.\nBrown GC, Borutaite V: There is no evidence that mitochondria are the main source of reactive oxygen species in mammalian cells. Mitochondrion. 2012, 12: 1-14. 10.1016\u002Fj.mito.2011.02.001.\nHickey AJ, Jüllig M, Aitken J, Loomes K, Hauber ME, Phillips AR: Birds and longevity: does flight driven aerobicity provide an oxidative sink?. Ageing Res Rev. 2012, 11: 242-253. 10.1016\u002Fj.arr.2011.12.002.\nRistow M, Schmeisser S: Extending life span by increasing oxidative stress. Free Radical Biol Med. 2011, 51: 327-336. 10.1016\u002Fj.freeradbiomed.2011.05.010.\nWeisiger RA, Fridovich I: Mitochondrial superoxide dismutase: site of synthesis and intramitochondrial localization. J Biol Chem. 1973, 248: 4793-4796.\nFridovich I: Superoxide radical and superoxide dismutases. Annu Rev Biochem. 1995, 64: 97-112. 10.1146\u002Fannurev.bi.64.070195.000525.\nOkado-Matsumoto A, Fridovich I: Subcellular distribution of superoxide dismutases (SOD) in rat liver: Cu, ZnSOD in mitochondria. J Biol Chem. 2001, 276: 28388-28393. 10.1074\u002Fjbc.M100605200.\nMargis R, Dunand C, Teixeira FK, Margis-Pinheiro M: Glutathione peroxidase family – an evolutionary overview. FEBS J. 2008, 275: 3959-3970. 10.1111\u002Fj.1742-4658.2008.06542.x.\nCox AG, Winterbourn CC, Hampton MB: Mitochondrial peroxiredoxin involvement in antioxidant defence and redox signaling. Biochem J. 2009, 425: 313-325.\nMurphy MP: Mitochondrial thiols in antioxidant protection and redox signaling: distinct roles for glutathionylation and other thiol modifications. Antioxid Redox Signal. 2012, 15: 476-495.\nRindler PM, Plafker SM, Szweda L, Kinter M: High dietary fat selectively increases catalase expression within cardiac mitochondria. 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Age (Dordr). 2010, 32: 255-270. 10.1007\u002Fs11357-010-9131-2.\nSalway KD, Page MM, Faure PA, Burness G, Stuart JA: Enhanced protein repair and recycling are not correlated with longevity in 15 vertebrate endotherm species. Age (Dordr). 2011, 33: 33-47. 10.1007\u002Fs11357-010-9157-5.\nSalway KD, Gallagher EJ, Stuart JA: Longer-lived mammals and birds have higher levels of heat shock proteins. Mech Age Devel. 2011, 132: 287-297. 10.1016\u002Fj.mad.2011.06.002.\nJang YC, Van Remmen H: The mitochondrial theory of aging: insight from transgenic and knockout mouse models. Exp Gerontol. 2009, 44: 256-260. 10.1016\u002Fj.exger.2008.12.006.\nPérez VI, Van Remmen H, Bokov A, Epstein CJ, Vijg J, Richardson A: The overexpression of major antioxidant enzymes does not extend the lifespan of mice. Aging Cell. 2009, 8: 73-75. 10.1111\u002Fj.1474-9726.2008.00449.x.\nPérez VI, Bokov A, Van Remmen H, Mele J, Ran Q, Ikeno Y, Richardson A: Is the oxidative stress theory of aging dead?. Biochim Biophys Acta. 2009, 1790: 1005-1014. 10.1016\u002Fj.bbagen.2009.06.003.\nHu D, Cao P, Thiels E, Chu CT, Wu G, Oury TD, Klann E: Hippocampal long-term potentiation, memory, and longevity in mice that overexpress mitochondrial superoxide dismutase. Neurobiol Learn Mem. 2007, 87: 372-384. 10.1016\u002Fj.nlm.2006.10.003.\nVan Remmen H, Ikeno Y, Hamilton M, Pahlavani M, Wolf N, Thorpe SR, Alderson NL, Baynes JW, Epstein CJ, Huang T, Nelson J, Strong R, Richardson A: Life-long reduction in MnSOD activity results in increased DNA damage and higher incidence of cancer but does not accelerate aging. Physiol Genomics. 2003, 16: 29-37. 10.1152\u002Fphysiolgenomics.00122.2003.\nHuang T, Carlson EJ, Gillespie AM, Shi Y, Epstein CJ: Ubiquitous overexpression of CuZn superoxide dismutase does not extend life span in mice. J Gerontol A Biol Sci Med Sci. 2000, 55: B5-B9.\nElchuri S, Oberley TD, Qi W, Eisenstein RS, Jackson Roberts L, Van Remmen H, Epstein CJ, Huang T: CuZnSOD deficiency leads to persistent and widespread oxidative damage and hepatocarcinogenesis later in life. Oncogene. 2005, 24: 367-380. 10.1038\u002Fsj.onc.1208207.\nSchriner SE, Linford NJ, Martin GM, Treuting P, Ogburn CE, Emond M, Coskun PE, Ladiges W, Wolf N, Van Remmen H, Wallace DC, Rabinovitch PS: Extension of murine life span by overexpression of catalase targeted to mitochondria. Science. 2005, 308: 1909-1911. 10.1126\u002Fscience.1106653.\nRan Q, Liang H, Ikeno Y, Qi W, Prolla TA, Roberts LJ, Wolfe N, Van Remmen H, Richardson A: Reduction in glutathione peroxidase 4 increases life span through increased sensitivity to apoptosis. J Gerontol A Biol Sci Med Sci. 2007, 62: 932-942. 10.1093\u002Fgerona\u002F62.9.932.\nZhang Y, Ikeno Y, Qi W, Chaudhuri A, Li Y, Bokov A, Thorpe SR, Baynes JW, Epstein C, Richardson A, Van Remmen H: Mice deficient in both Mn superoxide dismutase and glutathione peroxidase-1 have increased oxidative damage and a greater incidence of pathology but no reduction in longevity. J Gerontol A Biol Sci Med Sci. 2009, 64: 1212-1220.\nPérez VI, Cortez LA, Lew CM, Rodriguez M, Webb CR, Van Remmen H, Chaudhuri A, Qi W, Lee S, Bokov A, Fok W, Jones D, Richardson A, Yodoi J, Zhang Y, Tominaga K, Hubbard GB, Ikeno Y: Thioredoxin 1 overexpression extends mainly the earlier part of life span in mice. J Gerontol A Biol Sci Med Sci. 2011, 66: 1286-1299.\nSalmon AB, Pérez VI, Bokov A, Jernigan A, Kim G, Zhao H, Levine RL, Richardson A: Lack of methionine sulfoxide reductase A in mice increases sensitivity to oxidative stress but does not diminish life span. FASEB J. 2009, 23: 3601-3608. 10.1096\u002Ffj.08-127415.\nMoskovitz J, Bar-Noy S, Williams WM, Requena J, Berlett BS, Stadtman ER: Methionine sulfoxide reductase (MsrA) is a regulator of antioxidant defense and lifespan in mammals. Proc Natl Acad Sci U S A. 2001, 98: 12920-12925. 10.1073\u002Fpnas.231472998.\nWanagat J, Dai DF, Rabinovitch P: Mitochondrial oxidative stress and mammalian healthspan. Mech Ageing Dev. 2010, 131: 527-535. 10.1016\u002Fj.mad.2010.06.002.\nErnst IM, Pallauf K, Bendall JK, Paulsen L, Nikolai S, Huebbe P, Roeder T, Rimbach G: Vitamin E supplementation and lifespan in model organisms. Ageing Res Rev. 2013, 12: 365-375. 10.1016\u002Fj.arr.2012.10.002.\nBjelakovic G, Nikolova D, Gluud LL, Simonetti RG, Gluud C: Antioxidant supplements for prevention of mortality in healthy participants and patients with various diseases. Cochrane Database Syst Rev. 2012, 3: CD007176\nStuart JA, Robb EL: Health effects of resveratrol and its derivatives. Bioactive Polyphenols from Wine Grapes. SpringerBriefs in Cell Biology. 2013, New York, NY, USA: Springer Press, 9-25.\nMagwere T, West M, Riyahi K, Murphy MP, Smith RA, Partridge L: The effects of exogenous antioxidants on lifespan and oxidative stress resistance in Drosophila melanogaster. Mech Ageing Dev. 2006, 127: 356-370. 10.1016\u002Fj.mad.2005.12.009.\nRodriguez-Cuenca S, Cocheme HM, Logan A, Abakumova I, Prime TA, Rose C, Vidal-Puig A, Smith AC, Rubinsztein DC, Fearnley IM, Jones BA, Pope S, Heales SJ, Lam BY, Neogi SG, McFarlane I, James AM, Smith RA, Murphy MP: Consequences of long-term oral administration of the mitochondria-targeted antioxidant MitoQ to wildtype mice. Free Radic Biol Med. 2010, 48: 161-172. 10.1016\u002Fj.freeradbiomed.2009.10.039.\nSelsby JT, Judge AR, Yimlamai T, Leeuwenburgh C, Dodd SL: Life long calorie restriction increases heat shock proteins and proteasome activity in soleus muscles of Fisher 344 rats. Exp Gerontol. 2005, 40: 37-42. 10.1016\u002Fj.exger.2004.08.012.\nHepple RT, Qin M, Nakamato H, Goto S: Caloric restriction optimizes the proteasome pathway with aging in rat plantaris muscle: implications for sarcopenia. Am J Physiol. 2008, 295: R1231-R1237.\nLi F, Zhang L, Craddock J, Bruce-Keller AJ, Dasuri K, Nguyen A, Keller JN: Aging and dietary restriction effects on ubiquitination, sumoylation, and the proteasome in the heart. Mech Ageing Dev. 2008, 129: 515-521. 10.1016\u002Fj.mad.2008.04.007.\nBonelii MA, Desenzani S, Cavallini G, Donati A, Romani AA, Bergamini E, Borghetti AF: Low-level caloric restriction rescues proteasome activity and Hsc70 level in liver of aged rats. Biogerontology. 2008, 9: 1-10. 10.1007\u002Fs10522-007-9111-9.\nPamplona R: Membrane phospholipids, lipoxidative damage and molecular integrity: a causal role in aging and longevity. Biochim Biophys Acta. 2008, 1777: 1249-1262. 10.1016\u002Fj.bbabio.2008.07.003.\nStuart JA, Liang P, Luo X, Page MM, Gallagher EJ, Christoff CA, Robb EL: A comparative cellular and molecular biology of longevity database. Age (Dordr). 2013, 35: 1937-1947. 10.1007\u002Fs11357-012-9458-y.\nVijg J, Suh Y: Genome instability and aging. Annu Rev Physiol. 2013, 75: 645-668. 10.1146\u002Fannurev-physiol-030212-183715.\nPage MM, Stuart JA: Activities of DNA base excision repair enzymes in liver and brain correlate with body mass, but not lifespan. Age (Dordr). 2012, 34: 1195-1209. 10.1007\u002Fs11357-011-9302-9.\nStuart JA, Bourque BM, de Souza-Pinto NC, Bohr VA: No evidence of mitochondrial respiratory dysfunction in OGG1-null mice deficient in removal of 8-oxodeoxyguanine from mitochondrial DNA. Free Radic Biol Med. 2005, 38: 737-745. 10.1016\u002Fj.freeradbiomed.2004.12.003.\nCabelof DC, Ikeno Y, Nyska A, Busuttil RA, Anyangwe N, Vijg J, Matherly LH, Tucker JD, Wilson SH, Richardson A, Heydari AR: Haploinsufficiency in DNA polymerase beta increases cancer risk with age and alters mortality rate. Cancer Res. 2006, 66: 7460-7465. 10.1158\u002F0008-5472.CAN-06-1177.\nPark S-H, Kang H-J, Kim H-S, Kim M-J, Heo J-I, Kim J-H, Kho Y-J, Kim SC, Kim J, Park J-B, Lee J-Y: Higher DNA repair activity is related with longer replicative life span in mammalian embryonic fibroblast cells. Biogerontology. 2011, 12: 565-579. 10.1007\u002Fs10522-011-9355-2.\nFinkel T: Signal transduction by reactive oxygen species. J Cell Biol. 2011, 194: 7-15. 10.1083\u002Fjcb.201102095.\nWinterbourn CC: The biological chemistry of hydrogen peroxide. Methods Enzymol. 2013, 528: 3-25.\nChouchani ET, Methner C, Nadtochiy SM, Logan A, Pell VR, Ding S, James AM, Cochemé HM, Reinhold J, Lilley KS, Partridge L, Fearnley IM, Robinson AJ, Hartley RC, Smith RA, Krieg T, Brookes PS, Murphy MP: Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I. Nat Med. 2013, 19: 753-759. 10.1038\u002Fnm.3212.\nCocheme HM, Murphy MP: Can antioxidants be effective therapeutics?. Curr Opin Investig Drugs. 2010, 11: 426-431.\nRhee SG: Cell signaling: H2O2, a necessary evil for cell signaling. Science. 2006, 312: 1882-1883. 10.1126\u002Fscience.1130481.\nRuiz-Gines JA, Lopez-Ongil S, Gonzalez-Rubio M, Gonzlez-Santiago L, Rodriguez-Puyol M, Rodriguez-Puyol D: Reactive oxygen species induce proliferation of bovine aortic endothelial cells. J Cardiovasc Pharmacol. 2000, 35: 109-113. 10.1097\u002F00005344-200001000-00014.\nFaucher K, Rabinovitch-Chable H, Barriere G, Cook-Moreau J, Rigaud M: Overexpression of cytosolic glutathione peroxidase (GPX1) delays endothelial cell growth and increases resistance to toxic challenges. Biochimie. 2003, 85: 611-617. 10.1016\u002FS0300-9084(03)00089-0.\nGoh J, Enns L, Fatemie S, Hopkins H, Morton J, Pettan-Brewer C, Ladiges W: Mitochondrial targeted catalase suppresses invasive breast cancer in mice. BMC Cancer. 2011, 11: 191-203. 10.1186\u002F1471-2407-11-191.\nSarsour EH, Venkataraman S, Kalen AL, Oberley LW, Goswami PC: Manganese superoxide dismutase activity regulates transitions between quiescent and proliferative growth. Aging Cell. 2008, 7: 405-417. 10.1111\u002Fj.1474-9726.2008.00384.x.\nOugh M, Lewis A, Zhang Y, Hinkhouse MM, Ritchie JM, Oberley LW, Cullen JJ: Inhibition of cell growth by overexpression of manganese superoxide dismutase (MnSOD) in human pancreatic carcinoma. Free Radic Res. 2004, 38: 1223-1233. 10.1080\u002F10715760400017376.\nVenkataraman S, Jiang X, Weydert C, Zhang Y, Zhang HJ, Goswami PC, Ritchie JM, Oberley LW, Buettner GR: Manganese superoxide dismutase overexpression inhibits the growth of androgen-independent prostate cancer cells. Oncogene. 2005, 24: 77-89. 10.1038\u002Fsj.onc.1208145.\nWeydert CJ, Waugh TA, Ritchie JM, Iyer KS, Smith JL, Li L, Spitz DR, Oberley LW: Overexpression of manganese or copper-zinc superoxide dismutase inhibits breast cancer growth. Free Radic Biol Med. 2006, 41: 226-237. 10.1016\u002Fj.freeradbiomed.2006.03.015.\nLi S, Yan T, Yang JQ, Oberley TD, Oberley LW: The role of cellular glutathione peroxidase redox regulation in the suppression of tumor cell growth by manganese superoxide dismutase. Cancer Res. 2000, 60: 3927-3939.\nSimsek T, Kocabas F, Zheng J, Deberardinis RJ, Mahmoud AI, Olson EN, Schneider JW, Zhang CC, Sadek HA: The distinct metabolic profile of hematopoietic stem cells reflects their location in a hypoxic niche. Cell Stem Cell. 2010, 7: 380-390. 10.1016\u002Fj.stem.2010.07.011.\nOwusu-Ansah E, Yavari A, Mandal S, Banerjee U: Distinct mitochondrial retrograde signals control the G1-S cell cycle checkpoint. Nat Genet. 2008, 40: 356-361. 10.1038\u002Fng.2007.50.\nIto K, Hirao A, Arai F, Takubo K, Matsuoka S, Miyamoto K, Ohmura M, Naka K, Hosokawa K, Ikeda Y, Suda T: Reactive oxygen species act through p38 MAPK to limit the lifespan of hematopoietic stem cells. Nat Med. 2006, 12: 446-451. 10.1038\u002Fnm1388.\nArmstrong L, Tilgner K, Saretzki G, Atkinson SP, Stojkovic M, Moreno R, Przyborski S, Lako M: Human induced pluripotent stem cell lines show stress defense mechanisms and mitochondrial regulation similar to those of human embryonic stem cells. Stem Cells. 2010, 28: 661-673. 10.1002\u002Fstem.307.\nChiu J, Dawes IW: Redox control of cell proliferation. Trends Cell Biol. 2012, 22: 592-601. 10.1016\u002Fj.tcb.2012.08.002.\nMaryanovich M, Gross A: A ROS rheostat for cell fate regulation. Trends Cell Biol. 2013, 23: 129-134. 10.1016\u002Fj.tcb.2012.09.007.",{"EN":804},"Since its inception more than four decades ago, the Mitochondrial Free Radical Theory of Aging (MFRTA) has served as a touchstone for research into the biology of aging. The MFRTA suggests that oxidative damage to cellular macromolecules caused by reactive oxygen species (ROS) originating from mitochondria accumulates in cells over an animal’s lifespan and eventually leads to the dysfunction and failure that characterizes aging. A central prediction of the theory is that the ability to ameliorate or slow this process should be associated with a slowed rate of aging and thus increased lifespan. A vast pool of data bearing on this idea has now been published. ROS production, ROS neutralization and macromolecule repair have all been extensively studied in the context of longevity. We review experimental evidence from comparisons between naturally long- or short-lived animal species, from calorie restricted animals, and from genetically modified animals and weigh the strength of results supporting the MFRTA. Viewed as a whole, the data accumulated from these studies have too often failed to support the theory. Excellent, well controlled studies from the past decade in particular have isolated ROS as an experimental variable and have shown no relationship between its production or neutralization and aging or longevity. Instead, a role for mitochondrial ROS as intracellular messengers involved in the regulation of some basic cellular processes, such as proliferation, differentiation and death, has emerged. If mitochondrial ROS are involved in the aging process, it seems very likely it will be via highly specific and regulated cellular processes and not through indiscriminate oxidative damage to macromolecules.",{"EN":806},"A midlife crisis for the mitochondrial free radical theory of aging",{"VOID":808},"10.1186\u002F2046-2395-3-4","https:\u002F\u002Flongevityandhealthspan.biomedcentral.com\u002Farticles\u002F10.1186\u002F2046-2395-3-4",[811,828,844,856],{"id":812,"sortIndex":102,"researcher":18,"roles":813,"affiliations":814,"properties":825},"873a772c-65c6-4759-b9fc-539ca43f8ef6",[508],[815],{"id":18,"sortIndex":19,"affiliation":816,"properties":18},{"id":817,"createTime":818,"updateTime":819,"relativeEntities":820,"slug":821,"properties":822,"entityType":92,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"16f7d4c8-f83d-4977-9a3f-6dc086c63d8f","2023-12-09T08:35:04.606+00:00","2024-10-09T14:07:17.123+00:00",[],"Department-of-Biological-Sciences-Brock-University-St-Catharines-Canada",{"title":823},{"VI":824},"Department of Biological Sciences, Brock University, St. Catharines, Canada",{"title":826},{"VI":827},"Lucas A Maddalena",{"id":829,"sortIndex":29,"researcher":18,"roles":830,"affiliations":831,"properties":841},"7ae28f4b-e0fc-43a1-b828-81f5cceede2f",[508],[832],{"id":18,"sortIndex":19,"affiliation":833,"properties":18},{"id":834,"createTime":835,"updateTime":835,"relativeEntities":836,"slug":837,"properties":838,"entityType":92,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"81986c48-7a0b-405b-9e40-2f739fd87ea4","2023-11-25T03:26:44.275+00:00",[],"Mitochondrial-Biology-Unit-Medical-Research-Council-Cambridge-UK",{"title":839},{"VI":840},"Mitochondrial Biology Unit, Medical Research Council, Cambridge, UK",{"title":842},{"VI":843},"Ellen L Robb",{"id":845,"sortIndex":19,"researcher":18,"roles":846,"affiliations":847,"properties":853},"da4fba2c-5692-4167-8468-88c6cf84d138",[508],[848],{"id":18,"sortIndex":19,"affiliation":849,"properties":18},{"id":817,"createTime":818,"updateTime":819,"relativeEntities":850,"slug":821,"properties":851,"entityType":92,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":852},{"VI":824},{"title":854},{"VI":855},"Jeffrey A Stuart",{"id":857,"sortIndex":79,"researcher":18,"roles":858,"affiliations":859,"properties":865},"271af43f-638a-4da3-ad7f-ebb5e2b0ad3a",[508],[860],{"id":18,"sortIndex":19,"affiliation":861,"properties":18},{"id":817,"createTime":818,"updateTime":819,"relativeEntities":862,"slug":821,"properties":863,"entityType":92,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":864},{"VI":824},{"title":866},{"VI":867},"Max Merilovich",{"url":809,"publisher":869,"properties":882},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":870,"slug":10,"properties":871,"entityType":16,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"subjectFields":874,"manageAffiliations":875,"indexDatabases":876,"url":18,"thumbnailPath":18,"statistic":877,"gsStatistic":18,"type":18,"analyzePriority":18},[],{"eissn":872,"title":873},{"VOID":13},{"EN":15},[],[],[],{"impactFactor":19,"impactFactorByYear":878,"i10Index":29,"i10IndexLast5Year":19,"totalPublication":30,"totalPublicationByYear":879,"totalCitation":35,"totalCitationByYear":880,"totalCitationPerPublication":40,"totalCitationPerPublicationByYear":881,"hindexLast5Year":29,"hindex":29},{"2013":25,"2014":26,"2015":27,"2016":28},{"2012":32,"2013":33,"2014":34},{"2012":37,"2013":38,"2014":39},{"2012":42,"2013":43,"2014":44},{"volume":883,"pages":885},{"VOID":884},"3",{"VOID":886},"1-15","2014-04-01",{"id":889,"createTime":890,"updateTime":891,"relativeEntities":892,"slug":893,"properties":894,"entityType":70,"verifyStatus":71,"verifyTime":891,"verifyNote":72,"syncStatus":17,"languages":910,"translateLanguages":18,"viewCount":19,"primaryUrl":911,"fullTextUrl":18,"authors":912,"publicationType":136,"publisherRelationship":1077,"citationCount":1094,"citationInfo":1095,"publishDate":1097,"publishYear":606,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":18,"openAccess":18,"references":1098,"isForceReanalyzing":487},"c02bdf36-c075-4e6a-b6c2-094c798dff75","2024-04-20T02:44:08.045+00:00","2025-02-26T19:44:56.322+00:00",[],"Lifelong-endurance-training-attenuates-age-related-genotoxic-stress-in-human-skeletal-muscle",{"mag":895,"keywords":897,"pmc":898,"openalex":900,"abstract":902,"title":904,"pm":906,"doi":908},{"VOID":896},"2159896896",{},{"VOID":899},"3922955",{"VOID":901},"W2159896896",{"EN":903},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\n          \u003Cjats:sec>\n            \u003Cjats:title>Background\u003C\u002Fjats:title>\n            \u003Cjats:p>The aim of the present study was to determine the influence of age and habitual activity level, at rest and following a single bout of high-intensity exercise, on the levels of three proteins poly(ADP-ribose) polymerase-1 (PARP-1), cleaved-PARP-1 and poly(ADP-ribose) glycohydrolase (PARG), involved in the DNA repair and cell death responses to stress and genotoxic insults. Muscle biopsies were obtained from the vastus lateralis of young trained (22 ± 3 years, \u003Cjats:italic>n\u003C\u002Fjats:italic> = 6), young untrained (24 ± 4 years, \u003Cjats:italic>n\u003C\u002Fjats:italic> = 6), old trained (64 ± 3 years, \u003Cjats:italic>n\u003C\u002Fjats:italic> = 6) and old untrained (65 ± 6 years, \u003Cjats:italic>n\u003C\u002Fjats:italic> = 6) healthy males before, immediately after and three days following a high-intensity interval exercise bout.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>\n          \u003Cjats:sec>\n            \u003Cjats:title>Results\u003C\u002Fjats:title>\n            \u003Cjats:p>PARP-1, which catalyzes poly(ADP-ribosyl)ation of proteins and DNA in response to a range of intrinsic and extrinsic stresses, was increased at baseline in old trained and old untrained compared with young trained and young untrained participants (\u003Cjats:italic>P\u003C\u002Fjats:italic> ≤ 0.05). Following exercise, PARP-1 levels remained unchanged in young trained participants, in contrast to old trained and old untrained where levels decreased and young untrained where levels increased (\u003Cjats:italic>P\u003C\u002Fjats:italic> ≤ 0.05). Interestingly, baseline levels of the cleaved PARP-1, a marker of apoptosis, and PARG, responsible for polymer degradation, were both significantly elevated in old untrained compared with old trained, young trained and young untrained (\u003Cjats:italic>P\u003C\u002Fjats:italic> ≤ 0.05). Despite this baseline difference in PARG, there was no change in any group following exercise. There was a non-significant statistical trend (\u003Cjats:italic>P\u003C\u002Fjats:italic> = 0.072) towards increased cleaved-PARP-1 expression post-exercise in younger but not old persons, regardless of training status.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>\n          \u003Cjats:sec>\n            \u003Cjats:title>Conclusions\u003C\u002Fjats:title>\n            \u003Cjats:p>Collectively, these results show that exercise slows the progression towards a chronically stressed state but has no impact on the age-related attenuated response to acute exercise. Our findings provide valuable insight into how habitual exercise training could protect skeletal muscle from chronic damage to macromolecules and may reduce sarcopenia in older people.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>",{"EN":905},"Lifelong endurance training attenuates age-related genotoxic stress in human skeletal muscle",{"VOID":907},"24472304",{"VOID":909},"10.1186\u002F2046-2395-2-11",[74],"https:\u002F\u002Flongevityandhealthspan.biomedcentral.com\u002Farticles\u002F10.1186\u002F2046-2395-2-11",[913,935,955,972,990,1010,1028,1045,1060],{"id":914,"sortIndex":915,"researcher":18,"roles":916,"affiliations":917,"properties":928},"9f1a06bd-8517-4fa2-a1c3-5d17b43eb534",5,[],[918],{"id":919,"sortIndex":19,"affiliation":920,"properties":18},"8148ee8d-9b7f-4b68-bf35-eeba9a089e9e",{"id":921,"createTime":922,"updateTime":922,"relativeEntities":923,"slug":924,"properties":925,"entityType":92,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"9fdaff38-ecd7-433a-8158-325177ec7834","2024-04-21T10:52:12.117+00:00",[],"Research-Institute-for-Sport-and-Exercise-Science-Liverpool-John-Moores-University-Liverpool-L3-3AF-UK",{"title":926},{"EN":927},"Research Institute for Sport and Exercise Science, Liverpool John Moores University, Liverpool, L3 3AF, UK",{"openalex":929,"orcid":931,"title":933},{"VOID":930},"A5048502906",{"VOID":932},"https:\u002F\u002Forcid.org\u002F0000-0001-7303-9318",{"EN":934},"Jatin G. Burniston",{"id":936,"sortIndex":79,"researcher":18,"roles":937,"affiliations":938,"properties":950},"09bb4522-6bf4-478a-a723-10623938f1b0",[],[939],{"id":940,"sortIndex":19,"affiliation":941,"properties":18},"dfdda5b2-1558-44ad-a991-bd02d0151be6",{"id":942,"createTime":943,"updateTime":944,"relativeEntities":945,"slug":946,"properties":947,"entityType":92,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"00e8e60c-4327-40ca-a5b0-b2136b357376","2024-01-29T00:45:23.240+00:00","2025-06-11T14:23:40.855+00:00",[],"Cardiology-Department-Liverpool-Heart-and-Chest-Hospital-Liverpool-L14-3PE-UK",{"title":948},{"VI":949},"Cardiology Department, Liverpool Heart and Chest Hospital, Liverpool L14 3PE, UK",{"openalex":951,"title":953},{"VOID":952},"A5002961007",{"EN":954},"Stephen P. 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EMBO J. 2002, 21: 4338-4348. 10.1093\u002Femboj\u002Fcdf433.\nMinty F, Thurlow JK, Harrison PR, Parkinson EK: Telomere dysfunction in human keratinocytes elicits senescence and a novel transcription profile. Exp Cell Res. 2008, 314: 2434-2447. 10.1016\u002Fj.yexcr.2008.05.007.\nZhang H, Zhao Q, Chen Y, Wang Y, Gao S, Mao Y, Li M, Peng A, He D, Xiao X: Selective expression of S100A7 in lung squamous cell carcinomas and large cell carcinomas but not in adenocarcinomas and small cell carcinomas. Thorax. 2008, 63: 352-359. 10.1136\u002Fthx.2007.087015.\nWang J, Sun Q, Morita Y, Jiang H, Gross A, Lechel A, Hildner K, Guachalla LM, Gompf A, Hartmann D, Schambach A, Wuestefeld T, Dauch D, Schrezenmeier H, Hofmann WK, Nakauchi H, Ju Z, Kestler HA, Zender L, Rudolph KL: A differentiation checkpoint limits hematopoietic stem cell self-renewal in response to DNA damage. Cell. 2012, 148: 1001-1014. 10.1016\u002Fj.cell.2012.01.040.\nRodier F, Coppe JP, Patil CK, Hoeijmakers WA, Munoz DP, Raza SR, Freund A, Campeau E, Davalos AR, Campisi J: Persistent DNA damage signalling triggers senescence-associated inflammatory cytokine secretion. Nat Cell Biol. 2009, 11: 973-979. 10.1038\u002Fncb1909.\nDulic V, Drullinger LF, Lees E, Reed SI, Stein GH: Altered regulation of G1 cyclins in senescent human diploid fibroblasts: accumulation of inactive cyclin E-Cdk2 and cyclin D1-Cdk2 complexes. Proc Natl Acad Sci U S A. 1993, 90: 11034-11038. 10.1073\u002Fpnas.90.23.11034.\nTopley GI, Okuyama R, Gonzales JG, Conti C, Dotto GP: p21(WAF1\u002FCip1) functions as a suppressor of malignant skin tumor formation and a determinant of keratinocyte stem-cell potential. Proc Natl Acad Sci U S A. 1999, 96: 9089-9094. 10.1073\u002Fpnas.96.16.9089.\nMissero C, Di Cunto F, Kiyokawa H, Koff A, Dotto GP: The absence of p21Cip1\u002FWAF1 alters keratinocyte growth and differentiation and promotes ras-tumor progression. Genes Dev. 1996, 10: 3065-3075. 10.1101\u002Fgad.10.23.3065.\nWolf R, Mirmohammadsadegh A, Walz M, Lysa B, Tartler U, Remus R, Hengge U, Michel G, Ruzicka T: Molecular cloning and characterization of alternatively spliced mRNA isoforms from psoriatic skin encoding a novel member of the S100 family. FASEB J. 2003, 17: 1969-1971.\nWolf R, Ruzicka T, Yuspa SH: Novel S100A7 (psoriasin)\u002FS100A15 (koebnerisin) subfamily: highly homologous but distinct in regulation and function. Amino Acids. 2011, 41: 789-796. 10.1007\u002Fs00726-010-0666-4.\nPanier S, Ichijima Y, Fradet-Turcotte A, Leung CC, Kaustov L, Arrowsmith CH, Durocher D: Tandem protein interaction modules organize the ubiquitin-dependent response to DNA double-strand breaks. 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Br J Cancer. 1999, 79: 47-53. 10.1038\u002Fsj.bjc.6690010.\nGschwandtner M, Zhong S, Tschachler A, Mlitz V, Karner S, Elbe-Burger A, Mildner M: Fetal human keratinocytes produce large amounts of antimicrobial peptides: involvement of histone-methylation processes. J Invest Dermatol. 2014, 134: 2192-2201. 10.1038\u002Fjid.2014.165.\nYu SE, Jang YK: The histone demethylase LSD1 is required for estrogen-dependent S100A7 gene expression in human breast cancer cells. Biochem Biophys Res Commun. 2012, 427: 336-342. 10.1016\u002Fj.bbrc.2012.09.057.\nSchoeftner S, Blanco R, Lopez De Silanes I, Munoz P, Gomez-Lopez G, Flores JM, Blasco MA: Telomere shortening relaxes X chromosome inactivation and forces global transcriptome alterations. Proc Natl Acad Sci U S A. 2009, 106: 19393-19398. 10.1073\u002Fpnas.0909265106.\nTomas-Loba A, Flores I, Fernandez-Marcos PJ, Cayuela ML, Maraver A, Tejera A, Borras C, Matheu A, Klatt P, Flores JM, Vina J, Serrano M, Blasco MA: Telomerase reverse transcriptase delays aging in cancer-resistant mice. Cell. 2008, 135: 609-622. 10.1016\u002Fj.cell.2008.09.034.\nGemenetzidis E, Bose A, Riaz AM, Chaplin T, Young BD, Ali M, Sugden D, Thurlow JK, Cheong SC, Teo SH, Wan H, Waseem A, Parkinson EK, Fortune F, Teh MT: FOXM1 upregulation is an early event in human squamous cell carcinoma and it is enhanced by nicotine during malignant transformation. PLoS One. 2009, 4: e4849-10.1371\u002Fjournal.pone.0004849.\nWolf R, Howard OM, Dong HF, Voscopoulos C, Boeshans K, Winston J, Divi R, Gunsior M, Goldsmith P, Ahvazi B, Chavakis T, Oppenheim JJ, Yuspa SH: Chemotactic activity of S100A7 (psoriasin) is mediated by the receptor for advanced glycation end products and potentiates inflammation with highly homologous but functionally distinct S100A15. J Immunol. 2008, 181: 1499-1506. 10.4049\u002Fjimmunol.181.2.1499.",{"EN":1274},"Replicative senescence is preceded by loss of repeat sequences of DNA from the telomeres that eventually leads to telomere dysfunction, the accumulation of irreparable DNA double strand breaks and a DNA damage response (DDR). However, we have previously reported that whilst telomere dysfunction in human keratinocytes is associated with a permanent cell cycle arrest, the DDR was very weak and transcriptional profiling also revealed several molecules normally associated with keratinocytes terminal differentiation, including S100A7 (psoriasin). We show here that S100A7 and the closely related S100A15 (koebnerisin) are not induced by repairable or irreparable DSBs, ruling out the hypotheses that these genes are induced either by the low DDR observed or by non-specific cell cycle arrest. We next tested whether S100A7 was induced by the cell cycle effectors ARF (p14ARF), CDKN2A (p16INK4A) and TP53 (p53) and found that, although all induced a similar level of acute and permanent cell cycle arrest to telomere dysfunction, none induced S100A7 (except p53 over-expression at high levels), showing that cell cycle arrest is not sufficient for its induction. The closely related transcript S100A15 was also upregulated by telomere dysfunction, to a similar extent by p16INK4A and p53 and to a lesser extent by p14ARF. Our results show that mere cell cycle arrest, the upregulation of senescence-associated cell cycle effectors and DNA damage are not sufficient for the induction of the S100 transcripts; they further suggest that whilst the induction of S100A15 expression is linked to both telomere-dependent and -independent senescence, S100A7 expression is specifically associated with telomere-dependent senescence in normal keratinocytes. As both S100A7 and S100A15 are secreted proteins, they may find utility in the early detection of human keratinocyte telomere dysfunction and senescence.",{"EN":1276},"The secreted protein S100A7 (psoriasin) is induced by telomere dysfunction in human keratinocytes independently of a DNA damage response and cell cycle regulators",{"VOID":1278},"10.1186\u002F2046-2395-3-8","https:\u002F\u002Flongevityandhealthspan.biomedcentral.com\u002Farticles\u002F10.1186\u002F2046-2395-3-8",[1281,1308,1323,1335,1347],{"id":1282,"sortIndex":974,"researcher":18,"roles":1283,"affiliations":1284,"properties":1305},"2007c300-f965-4092-8482-6d3d5dbb7803",[508],[1285,1297],{"id":1286,"sortIndex":102,"affiliation":1287,"properties":1296},"bae574ba-c306-45a4-981d-66ced96393c3",{"id":1288,"createTime":1289,"updateTime":1290,"relativeEntities":1291,"slug":1292,"properties":1293,"entityType":92,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"57df349b-0ed7-41bb-810d-322fef4c20c5","2024-01-12T20:36:16.411+00:00","2025-02-04T22:09:58.398+00:00",[],"London-UK",{"title":1294},{"VI":1295},"London, UK",{},{"id":18,"sortIndex":19,"affiliation":1298,"properties":18},{"id":1299,"createTime":1300,"updateTime":1300,"relativeEntities":1301,"slug":18,"properties":1302,"entityType":92,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"e5fb186f-19f2-40e2-b4db-02f2bc280e22","2024-02-11T19:06:01.457+00:00",[],{"title":1303},{"VI":1304},"Centre for Clinical & Diagnostic Oral Sciences, Institute of Dentistry, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, UK",{"title":1306},{"VI":1307},"Eric Kenneth Parkinson",{"id":1309,"sortIndex":29,"researcher":18,"roles":1310,"affiliations":1311,"properties":1320},"08b90c85-751c-41b5-b3b6-0514787a3caa",[508],[1312],{"id":18,"sortIndex":19,"affiliation":1313,"properties":18},{"id":1314,"createTime":1315,"updateTime":1315,"relativeEntities":1316,"slug":18,"properties":1317,"entityType":92,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"251d04da-4bd1-4602-9596-5edccb6cdf8b","2024-02-11T19:06:01.431+00:00",[],{"title":1318},{"VI":1319},"Department of Dermatology, Ludwig-Maximilian University Munich, Munich, Germany",{"title":1321},{"VI":1322},"Ronald 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Hattinger",{"id":1348,"sortIndex":102,"researcher":18,"roles":1349,"affiliations":1350,"properties":1356},"660f8cca-1039-4c0f-b88a-5dd72c556432",[508],[1351],{"id":18,"sortIndex":19,"affiliation":1352,"properties":18},{"id":1299,"createTime":1300,"updateTime":1300,"relativeEntities":1353,"slug":18,"properties":1354,"entityType":92,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":1355},{"VI":1304},{"title":1357},{"VI":1358},"Fay 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Br J Haematol. 2003, 123: 702-711. 10.1046\u002Fj.1365-2141.2003.04669.x.\nLiu B, Wang J, Chan KM, Tjia WM, Deng W, Guan X, Huang JD, Li KM, Chau PY, Chen DJ, Cao Y, Cheah KS, Tryggvason K, Zhou Z: Genomic instability in laminopathy-based premature aging. Nat Med. 2005, 11: 780-785. 10.1038\u002Fnm1266.\nSchneider CA, Rasband WS, Eliceiri KW: NIH Image to ImageJ: 25 years of image analysis. Nature methods. 2012, 9: 671-675. 10.1038\u002Fnmeth.2089.",{"EN":1388},"Alteration in the immune system is one of the most profound aspects of aging. Progressive changes in the number of B lymphocyte progenitors during aging have been reported but the underlying mechanisms are still elusive. A heterozygous G608G mutation in the LMNA gene leads to a deletion of 50 amino acids in lamin A protein, termed progerin, and is the predominant cause of Hutchinson-Gilford progeria syndrome (HGPS). Lack of Zmpste24, a metalloproteinase responsible for prelamin A processing, leads to progeroid features resembling HGPS. Therefore Zmpste24-deficient mice provide an ideal mouse model to study the impact of lamin A and (premature) aging on the aging-related decline of B lymphopoiesis. Analysis of bone marrow (BM) nucleated cells revealed a decline of early B cell progenitors in Zmpste24−\u002F− mice. BM transplantation in a congenic strain completely rescued the defects in B lymphopoiesis, indicating that the decline in B cell progenitors in Zmpste24−\u002F− mice is attributable to defective BM microenvironments rather than to cell-intrinsic defects. Further investigation revealed downregulation of a set of important early B lymphopoiesis factors in Zmpste24−\u002F− bone marrow stromal cells (BMSCs), such as Vcam-1, SDF-1α, Flt3L and TSLP, and most of them are under transcriptional control of NF-κB signaling. Though TNFα stimulates IκBα degradation and NF-κB nuclear translocation in Zmpste24−\u002F− BMSCs, NF-κB fails to stimulate IκBα re-expression, which mediates a negative feedback loop of NF-κB signaling in wild-type BMSCs. Our data demonstrate a cell-extrinsic defect of B cell development in a progeroid mouse model and a critical role for lamin A in the regulation of NF-κB signaling and cytokines that are essential for lymphopoiesis.",{"EN":1390},"Accumulation of prelamin A compromises NF-κB-regulated B-lymphopoiesis in a progeria mouse model",{"VOID":1392},"10.1186\u002F2046-2395-2-1","https:\u002F\u002Flongevityandhealthspan.biomedcentral.com\u002Farticles\u002F10.1186\u002F2046-2395-2-1",[1395,1410,1425,1437,1452,1464],{"id":1396,"sortIndex":102,"researcher":18,"roles":1397,"affiliations":1398,"properties":1407},"23dea89e-3677-4a3e-8d60-4b5ab76e746a",[508],[1399],{"id":18,"sortIndex":19,"affiliation":1400,"properties":18},{"id":1401,"createTime":1402,"updateTime":1402,"relativeEntities":1403,"slug":18,"properties":1404,"entityType":92,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"fd5fb14d-146e-409b-8760-945f97757126","2024-01-18T22:53:39.121+00:00",[],{"title":1405},{"VI":1406},"Department of Biochemistry, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong",{"title":1408},{"VI":1409},"Shuangcheng Zhou",{"id":1411,"sortIndex":79,"researcher":18,"roles":1412,"affiliations":1413,"properties":1422},"304ed7e5-a0c6-4e50-a189-4b6519883315",[508],[1414],{"id":18,"sortIndex":19,"affiliation":1415,"properties":18},{"id":1416,"createTime":1417,"updateTime":1417,"relativeEntities":1418,"slug":18,"properties":1419,"entityType":92,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"55441ac5-54f6-49b8-98d8-edb3360810ba","2023-12-20T17:18:27.245+00:00",[],{"title":1420},{"VI":1421},"Guangdong Medical College, Dongguan, China",{"title":1423},{"VI":1424},"Xinguang Liu",{"id":1426,"sortIndex":915,"researcher":18,"roles":1427,"affiliations":1428,"properties":1434},"7c9c06a5-f8ad-4d26-8029-acc2310806f6",[508],[1429],{"id":18,"sortIndex":19,"affiliation":1430,"properties":18},{"id":1401,"createTime":1402,"updateTime":1402,"relativeEntities":1431,"slug":18,"properties":1432,"entityType":92,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":1433},{"VI":1406},{"title":1435},{"VI":1436},"Zhongjun 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Zhang",{"id":1453,"sortIndex":29,"researcher":18,"roles":1454,"affiliations":1455,"properties":1461},"032d7595-daef-4c3f-a22a-8cc2c985fff9",[508],[1456],{"id":18,"sortIndex":19,"affiliation":1457,"properties":18},{"id":1416,"createTime":1417,"updateTime":1417,"relativeEntities":1458,"slug":18,"properties":1459,"entityType":92,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":1460},{"VI":1421},{"title":1462},{"VI":1463},"Keyuan Zhou",{"id":1465,"sortIndex":19,"researcher":18,"roles":1466,"affiliations":1467,"properties":1480},"725008ec-5435-4ca2-b3d2-21f7012fe3fe",[508],[1468,1473],{"id":18,"sortIndex":19,"affiliation":1469,"properties":18},{"id":1401,"createTime":1402,"updateTime":1402,"relativeEntities":1470,"slug":18,"properties":1471,"entityType":92,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":1472},{"VI":1406},{"id":1474,"sortIndex":102,"affiliation":1475,"properties":1479},"92414ea0-166a-4cf0-a585-e675fdbb4921",{"id":1416,"createTime":1417,"updateTime":1417,"relativeEntities":1476,"slug":18,"properties":1477,"entityType":92,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":1478},{"VI":1421},{},{"title":1481},{"VI":1482},"Baohua Liu",{"url":1393,"publisher":1484,"properties":1497},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1485,"slug":10,"properties":1486,"entityType":16,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"subjectFields":1489,"manageAffiliations":1490,"indexDatabases":1491,"url":18,"thumbnailPath":18,"statistic":1492,"gsStatistic":18,"type":18,"analyzePriority":18},[],{"eissn":1487,"title":1488},{"VOID":13},{"EN":15},[],[],[],{"impactFactor":19,"impactFactorByYear":1493,"i10Index":29,"i10IndexLast5Year":19,"totalPublication":30,"totalPublicationByYear":1494,"totalCitation":35,"totalCitationByYear":1495,"totalCitationPerPublication":40,"totalCitationPerPublicationByYear":1496,"hindexLast5Year":29,"hindex":29},{"2013":25,"2014":26,"2015":27,"2016":28},{"2012":32,"2013":33,"2014":34},{"2012":37,"2013":38,"2014":39},{"2012":42,"2013":43,"2014":44},{"volume":1498,"pages":1499},{"VOID":602},{"VOID":1500},"1-9","2013-01-02",{"id":1503,"createTime":1504,"updateTime":1505,"relativeEntities":1506,"slug":1507,"properties":1508,"entityType":70,"verifyStatus":71,"verifyTime":1505,"verifyNote":72,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"primaryUrl":1517,"fullTextUrl":18,"authors":1518,"publicationType":136,"publisherRelationship":1536,"citationCount":18,"citationInfo":18,"publishDate":1554,"publishYear":161,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":18,"openAccess":18,"references":18,"isForceReanalyzing":487},"57931333-d6a9-4257-b105-c3723ffb787f","2023-12-05T06:18:05.909+00:00","2025-02-19T16:40:54.946+00:00",[],"The-role-of-mitochondria-in-longevity-and-healthspan",{"references":1509,"abstract":1511,"title":1513,"doi":1515},{"VOID":1510},"Harman 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J Clin Endocrinol Metab. 2011, 96: 454-458. 10.1210\u002Fjc.2010-1167.",{"EN":1512},"The role of mitochondria in aging and disease remains contentious more than 40 years after the mitochondrial free radical theory of aging was first proposed. As part of a wider cross-journal series on contemporary mitochondrial biology, Longevity & Healthspan presents a thematic series of four reviews that discuss the evidence for and against the modern incarnations of the theory, and examine the relevance of mitochondrial membrane phospholipid unsaturation and the interactions of mitochondria with sex hormones.",{"EN":1514},"The role of mitochondria in longevity and healthspan",{"VOID":1516},"10.1186\u002F2046-2395-3-7","https:\u002F\u002Flongevityandhealthspan.biomedcentral.com\u002Farticles\u002F10.1186\u002F2046-2395-3-7",[1519],{"id":1520,"sortIndex":19,"researcher":18,"roles":1521,"affiliations":1522,"properties":1533},"a1456104-f6a3-4377-8636-fbcd6a19c00d",[508],[1523],{"id":18,"sortIndex":19,"affiliation":1524,"properties":18},{"id":1525,"createTime":1526,"updateTime":1527,"relativeEntities":1528,"slug":1529,"properties":1530,"entityType":92,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"09f5f5e9-5404-4f11-8079-881bf959f818","2024-01-09T22:44:12.111+00:00","2025-06-11T22:53:18.337+00:00",[],"The-Buck-Institute-for-Research-on-Aging-Novato-USA",{"title":1531},{"VI":1532},"The Buck Institute for Research on Aging, Novato, USA",{"title":1534},{"VI":1535},"Martin D Brand",{"url":1517,"publisher":1537,"properties":1550},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1538,"slug":10,"properties":1539,"entityType":16,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"subjectFields":1542,"manageAffiliations":1543,"indexDatabases":1544,"url":18,"thumbnailPath":18,"statistic":1545,"gsStatistic":18,"type":18,"analyzePriority":18},[],{"eissn":1540,"title":1541},{"VOID":13},{"EN":15},[],[],[],{"impactFactor":19,"impactFactorByYear":1546,"i10Index":29,"i10IndexLast5Year":19,"totalPublication":30,"totalPublicationByYear":1547,"totalCitation":35,"totalCitationByYear":1548,"totalCitationPerPublication":40,"totalCitationPerPublicationByYear":1549,"hindexLast5Year":29,"hindex":29},{"2013":25,"2014":26,"2015":27,"2016":28},{"2012":32,"2013":33,"2014":34},{"2012":37,"2013":38,"2014":39},{"2012":42,"2013":43,"2014":44},{"volume":1551,"pages":1552},{"VOID":884},{"VOID":1553},"1-3","2014-05-22",{"id":1556,"createTime":1557,"updateTime":1558,"relativeEntities":1559,"slug":1560,"properties":1561,"entityType":70,"verifyStatus":71,"verifyTime":1558,"verifyNote":72,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"primaryUrl":1570,"fullTextUrl":18,"authors":1571,"publicationType":136,"publisherRelationship":1683,"citationCount":18,"citationInfo":18,"publishDate":1701,"publishYear":606,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":18,"openAccess":18,"references":18,"isForceReanalyzing":487},"99293691-9858-4c35-8198-0cb7d7da010a","2023-12-28T13:36:01.582+00:00","2024-09-17T15:06:45.485+00:00",[],"Life-long-spontaneous-exercise-does-not-prolong-lifespan-but-improves-health-span-in-mice",{"references":1562,"abstract":1564,"title":1566,"doi":1568},{"VOID":1563},"Oeppen J, Vaupel JW: Demography. 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The aim of our study was to determine whether life-long spontaneous aerobic exercise affects lifespan and healthspan in mice. Male C57Bl\u002F6J mice, individually caged, were randomly assigned to one of two groups: sedentary (n = 72) or spontaneous wheel-runners (n = 72). We evaluated longevity and several health parameters including grip strength, motor coordination, exercise capacity (VO2max) and skeletal muscle mitochondrial biogenesis. We also measured the cortical levels of the brain-derived neurotrophic factor (BDNF), a neurotrophin associated with brain plasticity. In addition, we measured systemic oxidative stress (malondialdehyde and protein carbonyl plasma levels) and the expression and activity of two genes involved in antioxidant defense in the liver (that is, glutathione peroxidase (GPx) and manganese superoxide dismutase (Mn-SOD)). Genes that encode antioxidant enzymes are considered longevity genes because their over-expression may modulate lifespan. Aging was associated with an increase in oxidative stress biomarkers and in the activity of the antioxidant enzymes, GPx and Mn-SOD, in the liver in mice. Life-long spontaneous exercise did not prolong longevity but prevented several signs of frailty (that is, decrease in strength, endurance and motor coordination). This improvement was accompanied by a significant increase in the mitochondrial biogenesis in skeletal muscle and in the cortical BDNF levels. Life-long spontaneous exercise does not prolong lifespan but improves healthspan in mice. Exercise is an intervention that delays age-associated frailty, enhances function and can be translated into the clinic.",{"EN":1567},"Life-long spontaneous exercise does not prolong lifespan but improves health span in 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