Cardiac fibrosis and curcumin: a novel perspective on this natural medicine

Fatemeh Sadoughi1, Jamal Hallajzadeh2, Liaosadat Mirsafaei3, Zatollah Asemi1, Mahdi Zahedi4, Mohammad Alì Mansournia5, Bahman Yousefi6
1Research Center for Biochemistry and Nutrition in Metabolic Diseases, Institute for Basic Sciences, Kashan University of Medical Sciences, Kashan, Islamic Republic of Iran
2Department of Biochemistry and Nutrition, Medicinal Plants Research Center, Maragheh University of Medical Sciences, Maragheh, Iran
3Department of Cardiology, Ramsar Campus, Mazandaran University of Medical Sciences, Sari, Iran
4Ischemic Disorders Research Center, Golestan University of Medical Sciences, Gorgān, Iran
5Department of Epidemiology and Biostatistics, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
6Molecular Medicine Research Center, Tabriz University of Medical Sciences, Tabriz, Iran

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Kong P, Christia P, Frangogiannis NG (2014) The pathogenesis of cardiac fibrosis. Cell Mol Life Sci 71(4):549–574. https://doi.org/10.1007/s00018-013-1349-6

Ma ZG, Yuan YP, Wu HM, Zhang X, Tang QZ (2018) Cardiac fibrosis: new insights into the pathogenesis. Int J Biol Sci 14(12):1645–1657. https://doi.org/10.7150/ijbs.28103

Pellman J, Zhang J, Sheikh F (2016) Myocyte-fibroblast communication in cardiac fibrosis and arrhythmias: mechanisms and model systems. J Mol Cell Cardiol 94:22–31. https://doi.org/10.1016/j.yjmcc.2016.03.005

Nguyen MN, Kiriazis H, Gao XM, Du XJ (2017) Cardiac fibrosis and arrhythmogenesis. Compr Physiol 7(3):1009–1049. https://doi.org/10.1002/cphy.c160046

Frangogiannis NG (2019) Cardiac fibrosis: cell biological mechanisms, molecular pathways and therapeutic opportunities. Mol Aspects Med 65:70–99. https://doi.org/10.1016/j.mam.2018.07.001

Park S, Nguyen NB, Pezhouman A, Ardehali R (2019) Cardiac fibrosis: potential therapeutic targets. Transl Res 209:121–137. https://doi.org/10.1016/j.trsl.2019.03.001

Berk BC, Fujiwara K, Lehoux S (2007) ECM remodeling in hypertensive heart disease. J Clin Invest 117(3):568–575. https://doi.org/10.1172/JCI31044

Borer JS, Truter S, Herrold EM, Falcone DJ, Pena M, Carter JN, Dumlao TF, Lee JA, Supino PG (2002) Myocardial fibrosis in chronic aortic regurgitation: molecular and cellular responses to volume overload. Circulation 105(15):1837–1842. https://doi.org/10.1161/01.cir.0000014419.71706.85

Ashrafian H, McKenna WJ, Watkins H (2011) Disease pathways and novel therapeutic targets in hypertrophic cardiomyopathy. Circ Res 109(1):86–96. https://doi.org/10.1161/CIRCRESAHA.111.242974

Kania G, Blyszczuk P, Eriksson U (2009) Mechanisms of cardiac fibrosis in inflammatory heart disease. Trends Cardiovasc Med 19(8):247–252. https://doi.org/10.1016/j.tcm.2010.02.005

Fernandez-Sola J (2020) The effects of ethanol on the heart: alcoholic cardiomyopathy. Nutrients. https://doi.org/10.3390/nu12020572

Bharati S, Lev M (1995) Cardiac conduction system involvement in sudden death of obese young people. Am Heart J 129(2):273–281. https://doi.org/10.1016/0002-8703(95)90008-x

Asbun J, Villarreal FJ (2006) The pathogenesis of myocardial fibrosis in the setting of diabetic cardiomyopathy. J Am Coll Cardiol 47(4):693–700. https://doi.org/10.1016/j.jacc.2005.09.050

Espeland T, Lunde IG, Amundsen BH, Gullestad L, Aakhus S (2018) Myocardial fibrosis. Tidsskr Nor Laegeforen. https://doi.org/10.4045/tidsskr.17.1027

Lopez B, Gonzalez A, Ravassa S, Beaumont J, Moreno MU, San Jose G, Querejeta R, Diez J (2015) Circulating biomarkers of myocardial fibrosis: the need for a reappraisal. J Am Coll Cardiol 65(22):2449–2456. https://doi.org/10.1016/j.jacc.2015.04.026

Herum KM, Lunde IG, McCulloch AD, Christensen G (2017) The soft- and hard-heartedness of cardiac fibroblasts: mechanotransduction signaling pathways in fibrosis of the heart. J Clin Med. https://doi.org/10.3390/jcm6050053

Pulido-Moran M, Moreno-Fernandez J, Ramirez-Tortosa C, Ramirez-Tortosa M (2016) Curcumin and health. Molecules 21(3):264. https://doi.org/10.3390/molecules21030264

Kim Y, Clifton P (2018) Curcumin, cardiometabolic health and dementia. Int J Environ Res Public Health. https://doi.org/10.3390/ijerph15102093

Aggarwal BB, Kumar A, Bharti AC (2003) Anticancer potential of curcumin: preclinical and clinical studies. Anticancer Res 23(1/A):363–398

Jain SK, Rains J, Jones K (2006) Effect of curcumin on protein glycosylation, lipid peroxidation, and oxygen radical generation in human red blood cells exposed to high glucose levels. Free Radic Biol Med 41(1):92–96. https://doi.org/10.1016/j.freeradbiomed.2006.03.008

Lijnen P, Petrov V (2000) Induction of cardiac fibrosis by aldosterone. J Mol Cell Cardiol 32(6):865–879. https://doi.org/10.1006/jmcc.2000.1129

Hinz B, Phan SH, Thannickal VJ, Galli A, Bochaton-Piallat ML, Gabbiani G (2007) The myofibroblast: one function, multiple origins. Am J Pathol 170(6):1807–1816. https://doi.org/10.2353/ajpath.2007.070112

Moore-Morris T, Cattaneo P, Puceat M, Evans SM (2016) Origins of cardiac fibroblasts. J Mol Cell Cardiol 91:1–5. https://doi.org/10.1016/j.yjmcc.2015.12.031

Hawiger J, Zienkiewicz J (2019) Decoding inflammation, its causes, genomic responses, and emerging countermeasures. Scand J Immunol 90(6):e12812. https://doi.org/10.1111/sji.12812

Frangogiannis NG (2012) Regulation of the inflammatory response in cardiac repair. Circ Res 110(1):159–173. https://doi.org/10.1161/CIRCRESAHA.111.243162

Epelman S, Lavine KJ, Beaudin AE, Sojka DK, Carrero JA, Calderon B, Brija T, Gautier EL, Ivanov S, Satpathy AT (2014) Embryonic and adult-derived resident cardiac macrophages are maintained through distinct mechanisms at steady state and during inflammation. Immunity 40(1):91–104

Marone G, Lichtenstein LM, Galli FJ (2000) Mast cells and basophils. Academic Press, London

Barron L, Wynn TA (2011) Fibrosis is regulated by Th2 and Th17 responses and by dynamic interactions between fibroblasts and macrophages. Am J Physiol Gastrointest Liver Physiol 300(5):G723-728. https://doi.org/10.1152/ajpgi.00414.2010

Wynn TA (2008) Cellular and molecular mechanisms of fibrosis. J Pathol 214(2):199–210. https://doi.org/10.1002/path.2277

Hulsmans M, Sager HB, Roh JD, Valero-Muñoz M, Houstis NE, Iwamoto Y, Sun Y, Wilson RM, Wojtkiewicz G, Tricot B (2018) Cardiac macrophages promote diastolic dysfunction. J Exp Med 215(2):423–440

Falkenham A, de Antueno R, Rosin N, Betsch D, Lee TD, Duncan R, Légaré J-F (2015) Nonclassical resident macrophages are important determinants in the development of myocardial fibrosis. Am J Pathol 185(4):927–942

Zhang W, Chancey AL, Tzeng HP, Zhou Z, Lavine KJ, Gao F, Sivasubramanian N, Barger PM, Mann DL (2011) The development of myocardial fibrosis in transgenic mice with targeted overexpression of tumor necrosis factor requires mast cell-fibroblast interactions. Circulation 124(19):2106–2116. https://doi.org/10.1161/CIRCULATIONAHA.111.052399

Liao CH, Akazawa H, Tamagawa M, Ito K, Yasuda N, Kudo Y, Yamamoto R, Ozasa Y, Fujimoto M, Wang P, Nakauchi H, Nakaya H, Komuro I (2010) Cardiac mast cells cause atrial fibrillation through PDGF-A-mediated fibrosis in pressure-overloaded mouse hearts. J Clin Invest 120(1):242–253. https://doi.org/10.1172/JCI39942

Fairweather D, Frisancho-Kiss S, Yusung SA, Barrett MA, Davis SE, Gatewood SJ, Njoku DB, Rose NR (2004) Interferon-gamma protects against chronic viral myocarditis by reducing mast cell degranulation, fibrosis, and the profibrotic cytokines transforming growth factor-beta 1, interleukin-1 beta, and interleukin-4 in the heart. Am J Pathol 165(6):1883–1894. https://doi.org/10.1016/s0002-9440(10)63241-5

Kanellakis P, Ditiatkovski M, Kostolias G, Bobik A (2012) A pro-fibrotic role for interleukin-4 in cardiac pressure overload. Cardiovasc Res 95(1):77–85. https://doi.org/10.1093/cvr/cvs142

Levick SP, Widiapradja A (2018) Mast cells: key contributors to cardiac fibrosis. Int J Mol Sci. https://doi.org/10.3390/ijms19010231

Shiota N, Jin D, Takai S, Kawamura T, Koyama M, Nakamura N, Miyazaki M (1997) Chymase is activated in the hamster heart following ventricular fibrosis during the chronic stage of hypertension. FEBS Lett 406(3):301–304. https://doi.org/10.1016/s0014-5793(97)00295-0

Levick SP, McLarty JL, Murray DB, Freeman RM, Carver WE, Brower GL (2009) Cardiac mast cells mediate left ventricular fibrosis in the hypertensive rat heart. Hypertension 53(6):1041–1047. https://doi.org/10.1161/HYPERTENSIONAHA.108.123158

Matsuda N, Jesmin S, Takahashi Y, Hatta E, Kobayashi M, Matsuyama K, Kawakami N, Sakuma I, Gando S, Fukui H, Hattori Y, Levi R (2004) Histamine H1 and H2 receptor gene and protein levels are differentially expressed in the hearts of rodents and humans. J Pharmacol Exp Ther 309(2):786–795. https://doi.org/10.1124/jpet.103.063065

Silver RB, Reid AC, Mackins CJ, Askwith T, Schaefer U, Herzlinger D, Levi R (2004) Mast cells: a unique source of renin. Proc Natl Acad Sci USA 101(37):13607–13612. https://doi.org/10.1073/pnas.0403208101

Nevers T, Salvador AM, Velazquez F, Ngwenyama N, Carrillo-Salinas FJ, Aronovitz M, Blanton RM, Alcaide P (2017) Th1 effector T cells selectively orchestrate cardiac fibrosis in nonischemic heart failure. J Exp Med 214(11):3311–3329

Duerrschmid C, Trial J, Wang Y, Entman ML, Haudek SB (2015) Tumor necrosis factor: a mechanistic link between angiotensin-II-induced cardiac inflammation and fibrosis. Circ Heart Fail 8(2):352–361

Wells JM, Gaggar A, Blalock JE (2015) MMP generated matrikines. Matrix Biol 44–46:122–129. https://doi.org/10.1016/j.matbio.2015.01.016

Lindsey ML, Iyer RP, Jung M, DeLeon-Pennell KY, Ma Y (2016) Matrix metalloproteinases as input and output signals for post-myocardial infarction remodeling. J Mol Cell Cardiol 91:134–140. https://doi.org/10.1016/j.yjmcc.2015.12.018

Lindner D, Zietsch C, Becher PM, Schulze K, Schultheiss HP, Tschope C, Westermann D (2012) Differential expression of matrix metalloproteases in human fibroblasts with different origins. Biochem Res Int 2012:875742. https://doi.org/10.1155/2012/875742

Tao ZY, Cavasin MA, Yang F, Liu YH, Yang XP (2004) Temporal changes in matrix metalloproteinase expression and inflammatory response associated with cardiac rupture after myocardial infarction in mice. Life Sci 74(12):1561–1572. https://doi.org/10.1016/j.lfs.2003.09.042

DeLeon-Pennell KY, Meschiari CA, Jung M, Lindsey ML (2017) Matrix metalloproteinases in myocardial infarction and heart failure. Prog Mol Biol Transl Sci 147:75–100. https://doi.org/10.1016/bs.pmbts.2017.02.001

van Putten S, Shafieyan Y, Hinz B (2016) Mechanical control of cardiac myofibroblasts. J Mol Cell Cardiol 93:133–142. https://doi.org/10.1016/j.yjmcc.2015.11.025

Vander Ark A, Cao J, Li X (2018) TGF-beta receptors: in and beyond TGF-beta signaling. Cell Signal 52:112–120. https://doi.org/10.1016/j.cellsig.2018.09.002

Todorovic V, Jurukovski V, Chen Y, Fontana L, Dabovic B, Rifkin DB (2005) Latent TGF-beta binding proteins. Int J Biochem Cell Biol 37(1):38–41. https://doi.org/10.1016/j.biocel.2004.03.011

Biernacka A, Dobaczewski M, Frangogiannis NG (2011) TGF-beta signaling in fibrosis. Growth Factors 29(5):196–202. https://doi.org/10.3109/08977194.2011.595714

Annes JP, Munger JS, Rifkin DB (2003) Making sense of latent TGFbeta activation. J Cell Sci 116(Pt 2):217–224. https://doi.org/10.1242/jcs.00229

Zhang Y, Alexander PB, Wang XF (2017) TGF-beta family signaling in the control of cell proliferation and survival. Cold Spring Harb Perspect Biol. https://doi.org/10.1101/cshperspect.a022145

Derynck R, Zhang YE (2003) Smad-dependent and Smad-independent pathways in TGF-beta family signalling. Nature 425(6958):577–584. https://doi.org/10.1038/nature02006

Seay U, Sedding D, Krick S, Hecker M, Seeger W, Eickelberg O (2005) Transforming growth factor-beta-dependent growth inhibition in primary vascular smooth muscle cells is p38-dependent. J Pharmacol Exp Ther 315(3):1005–1012. https://doi.org/10.1124/jpet.105.091249

Zhang YE (2009) Non-Smad pathways in TGF-beta signaling. Cell Res 19(1):128–139. https://doi.org/10.1038/cr.2008.328

Meng XM, Nikolic-Paterson DJ, Lan HY (2016) TGF-beta: the master regulator of fibrosis. Nat Rev Nephrol 12(6):325–338. https://doi.org/10.1038/nrneph.2016.48

Furukawa F, Matsuzaki K, Mori S, Tahashi Y, Yoshida K, Sugano Y, Yamagata H, Matsushita M, Seki T, Inagaki Y, Nishizawa M, Fujisawa J, Inoue K (2003) p38 MAPK mediates fibrogenic signal through Smad3 phosphorylation in rat myofibroblasts. Hepatology 38(4):879–889. https://doi.org/10.1053/jhep.2003.50384

Henderson NC, Arnold TD, Katamura Y, Giacomini MM, Rodriguez JD, McCarty JH, Pellicoro A, Raschperger E, Betsholtz C, Ruminski PG, Griggs DW, Prinsen MJ, Maher JJ, Iredale JP, Lacy-Hulbert A, Adams RH, Sheppard D (2013) Targeting of alphav integrin identifies a core molecular pathway that regulates fibrosis in several organs. Nat Med 19(12):1617–1624. https://doi.org/10.1038/nm.3282

Wipff PJ, Rifkin DB, Meister JJ, Hinz B (2007) Myofibroblast contraction activates latent TGF-beta1 from the extracellular matrix. J Cell Biol 179(6):1311–1323. https://doi.org/10.1083/jcb.200704042

Klingberg F, Chow ML, Koehler A, Boo S, Buscemi L, Quinn TM, Costell M, Alman BA, Genot E, Hinz B (2014) Prestress in the extracellular matrix sensitizes latent TGF-beta1 for activation. J Cell Biol 207(2):283–297. https://doi.org/10.1083/jcb.201402006

Wang Z, Stuckey DJ, Murdoch CE, Camelliti P, Lip GYH, Griffin M (2018) Cardiac fibrosis can be attenuated by blocking the activity of transglutaminase 2 using a selective small-molecule inhibitor. Cell Death Dis 9(6):613. https://doi.org/10.1038/s41419-018-0573-2

Yang J, Savvatis K, Kang JS, Fan P, Zhong H, Schwartz K, Barry V, Mikels-Vigdal A, Karpinski S, Kornyeyev D, Adamkewicz J, Feng X, Zhou Q, Shang C, Kumar P, Phan D, Kasner M, Lopez B, Diez J, Wright KC, Kovacs RL, Chen PS, Quertermous T, Smith V, Yao L, Tschope C, Chang CP (2016) Targeting LOXL2 for cardiac interstitial fibrosis and heart failure treatment. Nat Commun 7:13710. https://doi.org/10.1038/ncomms13710

Turner NA (2016) Inflammatory and fibrotic responses of cardiac fibroblasts to myocardial damage associated molecular patterns (DAMPs). J Mol Cell Cardiol 94:189–200. https://doi.org/10.1016/j.yjmcc.2015.11.002

Patel S (2018) Danger-associated molecular patterns (DAMPs): the derivatives and triggers of inflammation. Curr Allergy Asthma Rep 18(11):63. https://doi.org/10.1007/s11882-018-0817-3

Engebretsen KV, Lunde IG, Strand ME, Waehre A, Sjaastad I, Marstein HS, Skrbic B, Dahl CP, Askevold ET, Christensen G, Bjornstad JL, Tonnessen T (2013) Lumican is increased in experimental and clinical heart failure, and its production by cardiac fibroblasts is induced by mechanical and proinflammatory stimuli. FEBS J 280(10):2382–2398. https://doi.org/10.1111/febs.12235

Engebretsen KV, Waehre A, Bjornstad JL, Skrbic B, Sjaastad I, Behmen D, Marstein HS, Yndestad A, Aukrust P, Christensen G, Tonnessen T (2013) Decorin, lumican, and their GAG chain-synthesizing enzymes are regulated in myocardial remodeling and reverse remodeling in the mouse. J Appl Physiol 114(8):988–997. https://doi.org/10.1152/japplphysiol.00793.2012

Mansouri R, Hay E, Marie PJ, Modrowski D (2015) Role of syndecan-2 in osteoblast biology and pathology. Bonekey Rep 4:666. https://doi.org/10.1038/bonekey.2015.33

Elfenbein A, Simons M (2013) Syndecan-4 signaling at a glance. J Cell Sci 126(Pt 17):3799–3804. https://doi.org/10.1242/jcs.124636

Finsen AV, Lunde IG, Sjaastad I, Ostli EK, Lyngra M, Jarstadmarken HO, Hasic A, Nygard S, Wilcox-Adelman SA, Goetinck PF, Lyberg T, Skrbic B, Florholmen G, Tonnessen T, Louch WE, Djurovic S, Carlson CR, Christensen G (2011) Syndecan-4 is essential for development of concentric myocardial hypertrophy via stretch-induced activation of the calcineurin-NFAT pathway. PLoS ONE 6(12):e28302. https://doi.org/10.1371/journal.pone.0028302

Gopal S, Sogaard P, Multhaupt HA, Pataki C, Okina E, Xian X, Pedersen ME, Stevens T, Griesbeck O, Park PW, Pocock R, Couchman JR (2015) Transmembrane proteoglycans control stretch-activated channels to set cytosolic calcium levels. J Cell Biol 210(7):1199–1211. https://doi.org/10.1083/jcb.201501060

Weber KT, Sun Y, Bhattacharya SK, Ahokas RA, Gerling IC (2013) Myofibroblast-mediated mechanisms of pathological remodelling of the heart. Nat Rev Cardiol 10(1):15–26. https://doi.org/10.1038/nrcardio.2012.158

Kawano H, Do YS, Kawano Y, Starnes V, Barr M, Law RE, Hsueh WA (2000) Angiotensin II has multiple profibrotic effects in human cardiac fibroblasts. Circulation 101(10):1130–1137. https://doi.org/10.1161/01.cir.101.10.1130

Kim JA, Berliner JA, Nadler JL (1996) Angiotensin II increases monocyte binding to endothelial cells. Biochem Biophys Res Commun 226(3):862–868. https://doi.org/10.1006/bbrc.1996.1441

Maulik SK, Kumar S (2012) Oxidative stress and cardiac hypertrophy: a review. Toxicol Mech Methods 22(5):359–366. https://doi.org/10.3109/15376516.2012.666650

Klaunig JE (2018) Oxidative stress and cancer. Curr Pharm Des 24(40):4771–4778. https://doi.org/10.2174/1381612825666190215121712

Mallat Z, Philip I, Lebret M, Chatel D, Maclouf J, Tedgui A (1998) Elevated levels of 8-iso-prostaglandin F2α in pericardial fluid of patients with heart failure: a potential role for in vivo oxidant stress in ventricular dilatation and progression to heart failure. Circulation 97(16):1536–1539

Hill MF, Singal PK (1996) Antioxidant and oxidative stress changes during heart failure subsequent to myocardial infarction in rats. Am J Pathol 148(1):291

Li JM, Gall NP, Grieve DJ, Chen M, Shah AM (2002) Activation of NADPH oxidase during progression of cardiac hypertrophy to failure. Hypertension 40(4):477–484. https://doi.org/10.1161/01.hyp.0000032031.30374.32

Zhao W, Zhao T, Chen Y, Ahokas RA, Sun Y (2008) Oxidative stress mediates cardiac fibrosis by enhancing transforming growth factor-beta1 in hypertensive rats. Mol Cell Biochem 317(1–2):43–50. https://doi.org/10.1007/s11010-008-9803-8

Lijnen P, Papparella I, Petrov V, Semplicini A, Fagard R (2006) Angiotensin II-stimulated collagen production in cardiac fibroblasts is mediated by reactive oxygen species. J Hypertens 24(4):757–766

Siwik DA, Colucci WS (2004) Regulation of matrix metalloproteinases by cytokines and reactive oxygen/nitrogen species in the myocardium. Heart Fail Rev 9(1):43–51

Singh K, Balligand J-L, Fischer TA, Smith TW, Kelly RA (1996) Regulation of cytokine-inducible nitric oxide synthase in cardiac myocytes and microvascular endothelial cells role of extracellular signal-regulated kinases 1 and 2 (ERK1/ERK2) and STAT1α. J Biol Chem 271(2):1111–1117

Sugden PH, Clerk A (1998) “Stress-responsive” mitogen-activated protein kinases (c-Jun N-terminal kinases and p38 mitogen-activated protein kinases) in the myocardium. Circ Res 83(4):345–352

Xiao J, Sheng X, Zhang X, Guo M, Ji X (2016) Curcumin protects against myocardial infarction-induced cardiac fibrosis via SIRT1 activation in vivo and in vitro. Drug Des Dev Ther 10:1267

Wang NP, Wang ZF, Tootle S, Philip T, Zhao ZQ (2012) Curcumin promotes cardiac repair and ameliorates cardiac dysfunction following myocardial infarction. Br J Pharmacol 167(7):1550–1562

Ma J, Ma SY, Ding CH (2017) Curcumin reduces cardiac fibrosis by inhibiting myofibroblast differentiation and decreasing transforming growth factor beta1 and matrix metalloproteinase 9/tissue inhibitor of metalloproteinase 1. Chin J Integr Med 23(5):362–369. https://doi.org/10.1007/s11655-015-2159-5

Bugyei-Twum A, Ford C, Civitarese R, Seegobin J, Advani SL, Desjardins J-F, Kabir G, Zhang Y, Mitchell M, Switzer J (2018) Sirtuin 1 activation attenuates cardiac fibrosis in a rodent pressure overload model by modifying Smad2/3 transactivation. Cardiovasc Res 114(12):1629–1641

Liu H, Liu A, Shi C, Li B (2016) Curcumin suppresses transforming growth factor-β1-induced cardiac fibroblast differentiation via inhibition of Smad-2 and p38 MAPK signaling pathways. Exp Ther Med 11(3):998–1004

Zeng C, Zhong P, Zhao Y, Kanchana K, Zhang Y, Khan ZA, Chakrabarti S, Wu L, Wang J, Liang G (2015) Curcumin protects hearts from FFA-induced injury by activating Nrf2 and inactivating NF-κB both in vitro and in vivo. J Mol Cell Cardiol 79:1–12

Soetikno V, Sari FR, Sukumaran V, Lakshmanan AP, Mito S, Harima M, Thandavarayan RA, Suzuki K, Nagata M, Takagi R (2012) Curcumin prevents diabetic cardiomyopathy in streptozotocin-induced diabetic rats: possible involvement of PKC–MAPK signaling pathway. Eur J Pharm Sci 47(3):604–614

Gbr AA, Abdel Baky NA, Mohamed EA, Zaky HS (2021) Cardioprotective effect of pioglitazone and curcumin against diabetic cardiomyopathy in type 1 diabetes mellitus: impact on CaMKII/NF-κB/TGF-β1 and PPAR-γ signaling pathway. Naunyn Schmiedebergs Arch Pharmacol 394(2):349–360. https://doi.org/10.1007/s00210-020-01979-y

Yu W, Wu J, Cai F, Xiang J, Zha W, Fan D, Guo S, Ming Z, Liu C (2012) Curcumin alleviates diabetic cardiomyopathy in experimental diabetic rats. PLoS ONE 7(12):e52013

Lin J, Tang Y, Kang Q, Feng Y, Chen A (2012) Curcumin inhibits gene expression of receptor for advanced glycation end-products (RAGE) in hepatic stellate cells in vitro by elevating PPARγ activity and attenuating oxidative stress. Br J Pharmacol 166(8):2212–2227. https://doi.org/10.1111/j.1476-5381.2012.01910.x

Pang X-F, Zhang L-H, Bai F, Wang N-P, Garner RE, McKallip RJ, Zhao Z-Q (2015) Attenuation of myocardial fibrosis with curcumin is mediated by modulating expression of angiotensin II AT1/AT2 receptors and ACE2 in rats. Drug Des Dev Ther 9:6043

Hu J, Shen T, Xie J, Wang S, He Y, Zhu F (2017) Curcumin modulates covalent histone modification and TIMP1 gene activation to protect against vascular injury in a hypertension rat model. Exp Ther Med 14(6):5896–5902

Meng Z, Yu X-h, Chen J, Li L, Li S (2014) Curcumin attenuates cardiac fibrosis in spontaneously hypertensive rats through PPAR-γ activation. Acta Pharmacol Sin 35(10):1247–1256

Chung C-C, Kao Y-H, Liou J-P, Chen Y-J (2014) Curcumin suppress cardiac fibroblasts activities by regulating proliferation, migration, and the extracellular matrix. Acta Cardiol Sin 30(5):474

Guo S, Meng X-w, Yang X-s, Liu X-f, Ou-Yang C-h, Liu C (2018) Curcumin administration suppresses collagen synthesis in the hearts of rats with experimental diabetes. Acta Pharmacol Sin 39(2):195–204

Liu R, Zhang HB, Yang J, Wang JR, Liu JX, Li CL (2018) Curcumin alleviates isoproterenol-induced cardiac hypertrophy and fibrosis through inhibition of autophagy and activation of mTOR. Eur Rev Med Pharmacol Sci 22(21):7500–7508. https://doi.org/10.26355/eurrev_201811_16291

Rahnavard M, Hassanpour M, Ahmadi M, Heidarzadeh M, Amini H, Javanmard MZ, Nouri M, Rahbarghazi R, Safaie N (2019) Curcumin ameliorated myocardial infarction by inhibition of cardiotoxicity in the rat model. J Cell Biochem 120(7):11965–11972

Bellezza I, Giambanco I, Minelli A, Donato R Nrf2-Keap1 signaling in oxidative and reductive stress. Biochem Biophys Acta 1865(5):721–733. https://doi.org/10.1016/j.bbamcr.2018.02.010

Wu X, Huang L, Zhou X, Liu J (2020) Curcumin protects cardiomyopathy damage through inhibiting the production of reactive oxygen species in type 2 diabetic mice. Biochem Biophys Res Commun 530(1):15–21. https://doi.org/10.1016/j.bbrc.2020.05.053

Singh P, Hanson PS, Morris CM (2017) SIRT1 ameliorates oxidative stress induced neural cell death and is down-regulated in Parkinson’s disease. BMC Neurosci 18(1):46. https://doi.org/10.1186/s12868-017-0364-1

Peng T, Lu X, Feng Q (2005) Pivotal role of gp91 phox-containing NADH oxidase in lipopolysaccharide-induced tumor necrosis factor-α expression and myocardial depression. Circulation 111(13):1637–1644

Lipton JO, Sahin M (2014) The neurology of mTOR. Neuron 84(2):275–291. https://doi.org/10.1016/j.neuron.2014.09.034

Tanida I, Ueno T, Kominami E (2008) LC3 and autophagy. Methods Mol Biol 445:77–88. https://doi.org/10.1007/978-1-59745-157-4_4

Unlu A, Nayir E, Dogukan Kalenderoglu M, Kirca O, Ozdogan M (2016) Curcumin (turmeric) and cancer. J BUON 21(5):1050–1060