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Cigarette smoke exposure and a low dose of angiotensin II cooperatively induced severe hypertension in wild-type mice, but the scavenging of mitochondrial H\u003Cjats:sub>2\u003C\u002Fjats:sub>O\u003Cjats:sub>2\u003C\u002Fjats:sub> in mCAT mice completely prevented the development of hypertension. Cigarette smoke and angiotensin II cooperatively induced oxidation of cardiolipin (a specific biomarker of mitochondrial oxidative stress) in wild-type mice, which was abolished in mCAT mice. Cigarette smoke and angiotensin II impaired endothelium-dependent relaxation and induced superoxide overproduction, which was diminished in mCAT mice. To mimic the tobacco smoke exposure, we used cigarette smoke condensate, which induced mitochondrial superoxide overproduction and reduced endothelial nitric oxide (a hallmark of endothelial dysfunction in hypertension). Western blot experiments indicated that tobacco smoke and angiotensin II reduce the mitochondrial deacetylase sirtuin-3 level and cause hyperacetylation of a key mitochondrial antioxidant, SOD2, which promotes mitochondrial oxidative stress. \u003C\u002Fjats:p>\u003Cjats:p> NEW & NOTEWORTHY This work demonstrates tobacco smoking-induced mitochondrial oxidative stress, which contributes to endothelial dysfunction and development of hypertension. 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Previous studies have demonstrated a discrete population of midmyocardial (M) cells in the ventricular myocardium having excessive action potential duration (APD) prolongation during long activation cycle lengths (CL) and under the influence of APD-prolonging agents. However, M cells have not been found in other studies. Existing explanations for the discrepancies appear inadequate. We hypothesized that instead of being a discrete group, M cell behavior is functional and conditionally expressed. We mapped APDs on the cut-exposed transmural surfaces of arterially perfused ventricular wedges from 26 dogs during Na\u003Cjats:sup>+\u003C\u002Fjats:sup> current modification with anemone toxin II (ATX-II). Compared with the endocardium, APDs were not statistically different in the parallel layer having the longest mean APD (APD\u003Cjats:sub>L\u003C\u002Fjats:sub>) and were significantly shorter in the epicardium in the 26 wedges before ATX-II. ATX-II (≥5 nmol\u002Fl) prolonged APD heterogeneously (midmyocardium > endocardium > epicardium). The differences increased at longer CLs. ATX-II (20.0 nmol\u002Fl) shifted the APD\u003Cjats:sub>L\u003C\u002Fjats:sub> layer to 32 ± 6.2% (6 wedges, CL: 4,000 ms) of the transmural thickness from the (sub)endocardium (8.6 ± 7.2%, 26 wedges, ATX-II free). We detected the presence of M cell behavior (significantly longer APDs in the APD\u003Cjats:sub>L\u003C\u002Fjats:sub> layer than in the endocardium and epicardium, P ≤ 0.04, CL: 4,000 ms) in the 18 wedges having ≥5 nmol\u002Fl ATX-II but not ( P > 0.36) in the other 18 wedges having ≤2.5 nmol\u002Fl ATX-II. Both the position of the APD\u003Cjats:sub>L\u003C\u002Fjats:sub> layer and presence of M cell-like behavior were modulated by ATX-II. The dynamic spatial modulation indicates that M cell behavior is functional and only becomes manifest under suitable conditions. \u003C\u002Fjats:p>",{"EN":1362},"Functional and transmural modulation of M cell behavior in canine ventricular wall",{"VOID":1364},"15331367",{"VOID":1366},"10.1152\u002Fajpheart.00526.2004",[130],"https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fajpheart.00526.2004",[1370,1387,1404],{"id":1371,"sortIndex":25,"researcher":24,"roles":1372,"affiliations":1373,"properties":1382,"displayName":1384,"givenName":24,"familyName":24},"b6eb5060-2ed9-431e-8434-7d46b4f604d8",[],[1374],{"id":1375,"sortIndex":25,"affiliation":1376,"properties":24},"cd5e5f04-8ad6-45d0-a71a-4570b2aa665c",{"id":1375,"createTime":24,"updateTime":24,"relativeEntities":1377,"slug":24,"properties":1378,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1381,"statistic":24},[],{"title":1379},{"EN":1380},"Krannert Institute of Cardiology, Indiana University School of Medicine, and Department of Biomedical Engineering, Indiana University Purdue University Indianapolis, Indianapolis, Indiana 46202",[],{"title":1383,"openalex":1385},{"EN":1384},"Norihiro Ueda",{"VOID":1386},"A5105266826",{"id":1388,"sortIndex":152,"researcher":24,"roles":1389,"affiliations":1390,"properties":1397,"displayName":1401,"givenName":24,"familyName":24},"bb6dae11-0e97-4a64-aba9-0e3a4fb68674",[],[1391],{"id":1375,"sortIndex":25,"affiliation":1392,"properties":24},{"id":1375,"createTime":24,"updateTime":24,"relativeEntities":1393,"slug":24,"properties":1394,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1396,"statistic":24},[],{"title":1395},{"EN":1380},[],{"orcid":1398,"title":1400,"openalex":1402},{"VOID":1399},"https:\u002F\u002Forcid.org\u002F0000-0001-7141-6829",{"EN":1401},"Douglas P. 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Cytochalasin D reduces Ca2+ sensitivity and maximum tension via interactions with myofilaments in skinned rat cardiac myocytes. 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Cytoskeletal actin microfilaments and the transient outward potassium current in hypertrophied rat ventriculocytes. J Physiol 541.2: 411–421, 2002.",{"doi":1608},"10.1113\u002Fjphysiol.2002.019562",{"id":24,"text":1610,"url":24,"identifiers":1611},"10.1152\u002Fajpheart.1996.270.6.H2157",{"doi":1610},{"id":24,"text":1613,"url":24,"identifiers":1614},"10.1152\u002Fajpheart.00346.2003",{"doi":1613},{"id":1616,"createTime":1617,"updateTime":1618,"relativeEntities":1619,"slug":1620,"properties":1621,"entityType":125,"verifyStatus":126,"verifyTime":1617,"verifyNote":128,"languages":1636,"translateLanguages":24,"viewCount":25,"primaryUrl":1637,"fullTextUrl":24,"authors":1638,"publicationType":216,"publisherRelationship":1715,"citationCount":1768,"citationInfo":1769,"publishDate":1772,"publishYear":1770,"citationAnalyzeStatus":23,"lastCitationAnalyze":1618,"indexDatabases":1773,"openAccess":24,"references":1774,"isForceReanalyzing":279},"699b50c8-0f80-49f8-8108-55c0d9bad15e","2024-09-19T11:30:13.556+00:00","2026-04-24T12:19:23.547+00:00",[],"Voluntary-exercise-delays-heart-failure-onset-in-rats-with-pulmonary-artery-hypertension",{"mag":1622,"gsPaper":1624,"openalex":1626,"abstract":1628,"title":1630,"pm":1632,"doi":1634},{"VOID":1623},"1946656077",{"VOID":1625},"[\"7585592779131007386\"]",{"VOID":1627},"W1946656077",{"EN":1629},"\u003Cjats:p> Increased physical activity is recommended for the general population and for patients with many diseases because of its health benefits but can be contraindicated if it is thought to be a risk for serious cardiovascular events. One such condition is pulmonary artery hypertension (PAH). PAH and right ventricular failure was induced in rats by a single injection of monocrotaline (MCT). MCT rats with voluntary access to a running wheel ran on average 2 km\u002Fday. The time for half the animals to develop heart failure signs (median survival time) was 28 days (exercise failure group), significantly longer than sedentary animals (sedentary failure group, 23 days). The contractility of single failing myocytes in response to increasing demand (stimulation frequency) was significantly impaired compared with that in both sedentary control and exercising control myocytes. However, myocytes from exercising MCT rats, tested at 23 days (exercise + MCT group), showed responses intermediate to the control (sedentary control and exercising control) and failing (sedentary failure and exercise failure) groups. We conclude that voluntary exercise is beneficial to rats with heart failure induced by PAH, and this is evidence to support the consideration of appropriate exercise regimes for potentially vulnerable groups. \u003C\u002Fjats:p>",{"EN":1631},"Voluntary exercise delays heart failure onset in rats with pulmonary artery hypertension",{"VOID":1633},"26001413",{"VOID":1635},"10.1152\u002Fajpheart.00262.2015",[130],"https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fajpheart.00262.2015",[1639,1660,1681,1698],{"id":1640,"sortIndex":25,"researcher":24,"roles":1641,"affiliations":1642,"properties":1651,"displayName":1655,"givenName":24,"familyName":24},"d8fb8709-7074-467b-aeba-9909d5602bf9",[],[1643],{"id":1644,"sortIndex":25,"affiliation":1645,"properties":24},"fb1ded88-6782-49e2-a668-0770f587887d",{"id":1644,"createTime":24,"updateTime":24,"relativeEntities":1646,"slug":24,"properties":1647,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1650,"statistic":24},[],{"title":1648},{"EN":1649},"Universidade Federal de Viçosa, Centro de Ciências Biológicas e da Saúde, Viçosa, Brasil; and",[],{"orcid":1652,"title":1654,"gsAuthor":1656,"openalex":1658},{"VOID":1653},"https:\u002F\u002Forcid.org\u002F0000-0002-4927-4024",{"EN":1655},"Antônio José Natali",{"VOID":1657},"[\"wg_-pswAAAAJ\"]",{"VOID":1659},"A5032517687",{"id":1661,"sortIndex":152,"researcher":24,"roles":1662,"affiliations":1663,"properties":1672,"displayName":1676,"givenName":24,"familyName":24},"15f2530a-c26d-4dc9-895a-9fb87841a625",[],[1664],{"id":1665,"sortIndex":25,"affiliation":1666,"properties":24},"94061b84-b609-4d05-9ed9-9acb4964dedf",{"id":1665,"createTime":24,"updateTime":24,"relativeEntities":1667,"slug":24,"properties":1668,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1671,"statistic":24},[],{"title":1669},{"EN":1670},"2Multidisciplinary Cardiovascular Research Centre, University of Leeds, Leeds, United Kingdom",[],{"orcid":1673,"title":1675,"gsAuthor":1677,"openalex":1679},{"VOID":1674},"https:\u002F\u002Forcid.org\u002F0000-0001-5580-2156",{"EN":1676},"Ewan D. 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This study tested the concept that changes in breathing parameters account for modifications in respiratory-related blood pressure (BP) and R-R interval (RRI) variability during nocturnal sleep. BP (Finapres), electrocardiogram, respiration (Respitrace), and polygraphic sleep recordings were recorded continuously in 13 healthy men aged 18-37 yr. The transfer characteristics identified by coherence and gain measures between the calibrated thoraco-abdominal motion and the respiratory-related BP and RRI variability evidenced a consistent increase during transitions from wake to light sleep and from light to deep sleep but returned to waking levels during rapid-eye-movement sleep (P < 0.0001). These changes were related to the specific modifications occurring in the respiratory rate, tidal volume, and ribcage-to-abdominal motion ratio during the different sleep stages (0.28 < r < 0.39; P < 0.0001). This study demonstrates 1) that modifications in the breathing pattern account for 8-15% of the variance in the cardiorespiratory transfer, and 2) that respiratory modulation of vagal activity is not the main mechanism controlling the magnitude of the respiratory-related BP and RRI variability during sleep. \u003C\u002Fjats:p>",{"EN":1864},"Cardiorespiratory transfer during sleep: a study in healthy young 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pulmonary arterial systolic pressure (PASP) and right ventricular (RV) tricuspid annular plane systolic excursion (TAPSE; from the end of diastole to end-systole) are of basic relevance in the clinical follow-up of heart failure (HF) patients, carrying two- to threefold increase in cardiac risk when increased and reduced, respectively. We hypothesized that the relationship between TAPSE (longitudinal RV fiber shortening) and PASP (force generated by the RV) provides an index of in vivo RV length-force relationship, with their ratio better disclosing prognosis. Two hundred ninety-three HF patients with reduced (HFrEF, n = 247) or with preserved left ventricular (LV) ejection fraction (HFpEF, n = 46) underwent echo-Doppler studies and N-terminal pro-brain-type natriuretic peptide assessment and were tracked for adverse events. The median follow-up duration was 20.8 mo. TAPSE vs. PASP relationship showed a downward regression line shift in nonsurvivors who were more frequently presenting with higher PASP and lower TAPSE. HFrEF and HFpEF patients exhibited a similar distribution along the regression line. Given the TAPSE, PASP, and TAPSE-to-PASP ratio (TAPSE\u002FPASP) collinearity, separate Cox regression and Kaplan-Meier analyses were performed: one with TAPSE and PASP as individual measures, and the other combining them in ratio form. Hazard ratios for variables retained in the multivariate regression were as follows: TAPSE\u002FPASP <\u002F≥ 0.36 mm\u002FmmHg [hazard ratio (HR): 10.4, P < 0.001]; TAPSE <\u002F≥ 16 mm (HR: 5.1, P < 0.01); New York Heart Association functional class <\u002F≥ 3 (HR: 4.4, P < 0.001); E\u002Fe’ (HR: 4.1, P < 0.001). This study shows that the TAPSE vs. PASP relationship is shifted downward in nonsurvivors with a similar distribution in HFrEF and HFpEF, and their ratio improves prognostic resolution. The TAPSE vs. PASP relationship as a possible index of the length-force relationship may be a step forward for a more efficient RV function evaluation and is not affected by the quality of LV dysfunction.\u003C\u002Fjats:p>","\u003Cjats:p>Huyết áp tâm thu động mạch phổi (PASP) được xác định bằng siêu âm và độ kéo dài của mặt đệm van ba lá (TAPSE; từ cuối tâm trương đến cuối tâm thu) có ý nghĩa cơ bản trong việc theo dõi lâm sàng bệnh nhân suy tim (HF), khi tăng và giảm lần lượt có thể làm gia tăng nguy cơ tim mạch từ hai đến ba lần. Chúng tôi giả thuyết rằng mối quan hệ giữa TAPSE (sự rút ngắn sợi cơ thất phải theo chiều dọc) và PASP (lực do thất phải tạo ra) cung cấp một chỉ số về mối quan hệ giữa chiều dài và lực của thất phải trong cơ thể, với tỷ lệ của chúng sẽ làm rõ hơn được tiên lượng. Hai trăm chín mươi ba bệnh nhân suy tim với phân suất tống máu thất trái giảm (HFrEF, n = 247) hoặc bảo tồn (HFpEF, n = 46) đã tham gia nghiên cứu siêu âm Doppler và đánh giá peptide natri lợi niệu pro-B-type N-terminal và được theo dõi các sự kiện bất lợi. Thời gian theo dõi trung bình là 20.8 tháng. Mối quan hệ giữa TAPSE và PASP cho thấy một sự dịch chuyển đường hồi quy xuống trong nhóm không sống sót, nhóm này thường có PASP cao hơn và TAPSE thấp hơn. Bệnh nhân HFrEF và HFpEF có phân bố tương tự dọc theo đường hồi quy. Do tính đồng nhất của TAPSE, PASP, và tỷ lệ TAPSE\u002FPASP, các phân tích hồi quy Cox và Kaplan-Meier riêng biệt đã được thực hiện: một phân tích với TAPSE và PASP như các biện pháp riêng lẻ, và một phân tích kết hợp chúng ở dạng tỷ lệ. Tỷ lệ nguy cơ cho các biến số giữ lại trong hồi quy đa biến như sau: TAPSE\u002FPASP <\u002F≥ 0.36 mm\u002FmmHg [tỷ lệ nguy cơ (HR): 10.4, P < 0.001]; TAPSE <\u002F≥ 16 mm (HR: 5.1, P < 0.01); lớp chức năng New York Heart Association <\u002F≥ 3 (HR: 4.4, P < 0.001); E\u002Fe’ (HR: 4.1, P < 0.001). Nghiên cứu này cho thấy mối quan hệ giữa TAPSE và PASP dịch chuyển xuống trong nhóm không sống sót với phân bố tương tự ở HFrEF và HFpEF, và tỷ lệ của chúng cải thiện độ chính xác tiên lượng. Mối quan hệ giữa TAPSE và PASP như một chỉ số có thể về mối quan hệ giữa chiều dài và lực có thể là một bước tiến tới đánh giá chức năng thất phải hiệu quả hơn và không bị ảnh hưởng bởi chất lượng của rối loạn chức năng thất trái.\u003C\u002Fjats:p>",{"EN":2035,"VI":2036},"Tricuspid annular plane systolic excursion and pulmonary arterial systolic pressure relationship in heart failure: an index of right ventricular contractile function and prognosis","Mối quan hệ giữa độ kéo dài của mặt đệm van ba lá và huyết áp tâm thu động mạch phổi ở bệnh suy tim: một chỉ số của chức năng co bóp thất phải và tiên lượng",{"VOID":2038},"23997100",{"VOID":2040},"10.1152\u002Fajpheart.00157.2013",[130],[2043],"VI","https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fajpheart.00157.2013",[2046,2065,2084,2101,2118,2137,2156,2175],{"id":2047,"sortIndex":25,"researcher":24,"roles":2048,"affiliations":2049,"properties":2058,"displayName":2062,"givenName":24,"familyName":24},"e933c887-cad6-437c-af2c-2090a0b9475d",[],[2050],{"id":2051,"sortIndex":25,"affiliation":2052,"properties":24},"ba6ea477-bac6-445d-8e48-2ce7364d3559",{"id":2051,"createTime":24,"updateTime":24,"relativeEntities":2053,"slug":24,"properties":2054,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2057,"statistic":24},[],{"title":2055},{"EN":2056},"Heart Failure Unit, Department of Cardiology, University of Milano, Istituto Di Ricovero e Cura a Carattere Scientifico (IRCCS) Policlinico San Donato, Milano, 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cống, tưới não tại chỗ, vận chuyển mạch máu não, lưu lượng máu não, hàng rào máu-não",{"VOID":2373},"W2126205988",{"EN":2375,"VI":2376},"\u003Cjats:p> The right cerebral hemisphere of the rat was perfused in situ by retrograde infusion of HCO3 saline or blood into the right external carotid artery. Infusion rate was adjusted to minimize the contribution of systemic blood to flow in the hemisphere. During perfusion with whole or artificial blood, regional cerebral blood flow and blood volume were comparable to respective values in the conscious rat, whereas perfusion with HCO3 saline increased regional flow three- to fourfold due to the low viscosity of the saline perfusate. Perfusion with whole blood for 300 S or with HCO3 saline for 60 S did not alter the permeability of the blood-brain barrier. Cerebrovascular permeability coefficients of eight nonelectrolytes ranged from 10(-8) to 10(-4) cm X S-1 and were directly proportional to the octanol-water partition coefficient of the solute. Thus the in situ brain perfusion technique is a sensitive new method to study cerebrovascular transfer in the rat and permits absolute control of perfusate composition. \u003C\u002Fjats:p>","\u003Cjats:p> Bán cầu não bên phải của chuột cống đã được tưới máu tại chỗ thông qua việc bơm ngược dung dịch HCO3 hoặc máu vào động mạch cảnh ngoài bên phải. Tốc độ bơm đã được điều chỉnh để giảm thiểu sự đóng góp của máu toàn thân vào dòng chảy trong bán cầu. Trong quá trình tưới bằng máu toàn phần hoặc máu nhân tạo, lưu lượng máu não khu vực và thể tích máu tương đương với các giá trị tương ứng ở chuột cống có ý thức, trong khi tưới bằng dung dịch HCO3 đã làm tăng lưu lượng khu vực gấp ba đến bốn lần do độ nhớt thấp của dung dịch tưới máu. Việc tưới bằng máu toàn phần trong 300 giây hoặc bằng dung dịch HCO3 trong 60 giây không làm thay đổi tính thấm của hàng rào máu-não. Hệ số thấm mạch máu não của tám chất không điện ly dao động từ 10(-8) đến 10(-4) cm X giây-1 và tỷ lệ thuận trực tiếp với hệ số phân chia octanol-nước của chất tan. Do đó, kỹ thuật tưới máu não tại chỗ là một phương pháp nhạy cảm mới để nghiên cứu quá trình chuyển giao mạch máu não ở chuột cống và cho phép kiểm soát tuyệt đối thành phần dung dịch tưới.",{"EN":2378,"VI":2379},"An in situ brain perfusion technique to study cerebrovascular transport in the rat","Kỹ thuật tưới máu não tại chỗ để nghiên cứu vận chuyển mạch máu não ở chuột cống",{"VOID":2381},"6476141",{"VOID":2383},"10.1152\u002Fajpheart.1984.247.3.h484","2025-01-25T10:50:04.964+00:00","Author affiliation is blank",[130],[2043],"https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fajpheart.1984.247.3.H484",[2390,2399,2410],{"id":2391,"sortIndex":25,"researcher":24,"roles":2392,"affiliations":2393,"properties":2394,"displayName":2396,"givenName":24,"familyName":24},"1093b584-63de-4048-90d0-590f15ca4b8d",[],[],{"title":2395,"openalex":2397},{"EN":2396},"Yoshio Takasato",{"VOID":2398},"A5021983041",{"id":2400,"sortIndex":152,"researcher":24,"roles":2401,"affiliations":2402,"properties":2403,"displayName":2407,"givenName":24,"familyName":24},"d72b47e3-33d2-41d1-bfe4-cb865cdfe437",[],[],{"orcid":2404,"title":2406,"openalex":2408},{"VOID":2405},"https:\u002F\u002Forcid.org\u002F0000-0003-4660-2931",{"EN":2407},"С. И. Рапопорт",{"VOID":2409},"A5103333058",{"id":2411,"sortIndex":170,"researcher":24,"roles":2412,"affiliations":2413,"properties":2414,"displayName":2416,"givenName":24,"familyName":24},"57cc3396-2b04-4afe-aa3e-4946f63d2a33",[],[],{"title":2415,"openalex":2417},{"EN":2416},"Quentin R. Smith",{"VOID":2418},"A5110086509",{"url":24,"publisher":2420,"properties":2466},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":2421,"slug":10,"properties":2422,"entityType":22,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":25,"subjectFields":2427,"manageAffiliations":2440,"indexDatabases":2451,"url":99,"thumbnailPath":24,"statistic":24,"gsStatistic":24,"type":24,"analyzePriority":24},[],{"country":2423,"eissn":2424,"issn":2425,"title":2426},{"VOID":13},{"VOID":15},{"VOID":17},{"EN":19},[2428,2432,2436],{"id":28,"createTime":24,"updateTime":24,"relativeEntities":2429,"label":2430,"description":2431,"parentId":24,"standard":24,"scholarHubFieldId":24},[],{"EN":31},{},{"id":34,"createTime":24,"updateTime":24,"relativeEntities":2433,"label":2434,"description":2435,"parentId":24,"standard":24,"scholarHubFieldId":24},[],{"EN":37},{},{"id":40,"createTime":24,"updateTime":24,"relativeEntities":2437,"label":2438,"description":2439,"parentId":24,"standard":24,"scholarHubFieldId":24},[],{"EN":43},{},[2441,2446],{"id":47,"createTime":24,"updateTime":24,"relativeEntities":2442,"slug":24,"properties":2443,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2445,"statistic":24},[],{"title":2444},{"EN":51},[],{"id":54,"createTime":24,"updateTime":24,"relativeEntities":2447,"slug":24,"properties":2448,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2450,"statistic":24},[],{"title":2449},{"EN":58},[],[2452,2459],{"id":62,"indexDatabase":2453,"url":75,"indexYears":24,"academicFieldIds":2458,"indexDatabaseRanking":24},{"id":64,"createTime":24,"updateTime":24,"relativeEntities":2454,"label":2455,"description":2456,"key":71,"publicationTags":2457,"standard":24},[],{"EN":67,"VI":67},{"EN":69,"VI":70},[73,74],[77,78,79],{"id":81,"indexDatabase":2460,"url":92,"indexYears":93,"academicFieldIds":2465,"indexDatabaseRanking":98},{"id":83,"createTime":24,"updateTime":24,"relativeEntities":2461,"label":2462,"description":2463,"key":89,"publicationTags":2464,"standard":24},[],{"EN":86,"VI":86},{"EN":86,"VI":88},[91],[95,96,97],{"issue":2467,"pages":2468,"volume":2470},{"VOID":575},{"VOID":2469},"H484-H493",{"VOID":2471},"247",541,{"total":2472,"publishYear":2474,"statisticByYear":2475},1984,{"2012":2476,"2013":2252,"2014":2477,"2015":589,"2016":2476,"2017":2478,"2018":2479,"2019":422,"2020":492,"2021":1482,"2022":510,"2023":442,"2024":170},15,16,12,14,"1984-09-01",[73,98],[],{"id":2484,"createTime":2485,"updateTime":2486,"relativeEntities":2487,"slug":2488,"properties":2489,"entityType":125,"verifyStatus":126,"verifyTime":2485,"verifyNote":128,"languages":2507,"translateLanguages":2508,"viewCount":25,"primaryUrl":2509,"fullTextUrl":24,"authors":2510,"publicationType":216,"publisherRelationship":2666,"citationCount":2720,"citationInfo":2721,"publishDate":2734,"publishYear":2722,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":2735,"openAccess":24,"references":2736,"isForceReanalyzing":279},"c6e0c8b0-9968-4a57-b71c-309d2de6f2e1","2024-10-11T03:17:02.694+00:00","2025-02-15T13:09:05.776+00:00",[],"High-purity-human-induced-pluripotent-stem-cell-derived-cardiomyocytes-electrophysiological-properties-of-action-potentials-and-ionic-currents",{"mag":2490,"keywords":2492,"pmc":2493,"openalex":2495,"abstract":2497,"title":2500,"pm":2503,"doi":2505},{"VOID":2491},"2124929662",{"VI":2028},{"VOID":2494},"4116414",{"VOID":2496},"W2124929662",{"EN":2498,"VI":2499},"\u003Cjats:p> Human-induced pluripotent stem cells (hiPSCs) can differentiate into functional cardiomyocytes; however, the electrophysiological properties of hiPSC-derived cardiomyocytes have yet to be fully characterized. We performed detailed electrophysiological characterization of highly pure hiPSC-derived cardiomyocytes. Action potentials (APs) were recorded from spontaneously beating cardiomyocytes using a perforated patch method and had atrial-, nodal-, and ventricular-like properties. Ventricular-like APs were more common and had maximum diastolic potentials close to those of human cardiac myocytes, AP durations were within the range of the normal human electrocardiographic QT interval, and APs showed expected sensitivity to multiple drugs (tetrodotoxin, nifedipine, and E4031). Early afterdepolarizations (EADs) were induced with E4031 and were bradycardia dependent, and EAD peak voltage varied inversely with the EAD take-off potential. Gating properties of seven ionic currents were studied including sodium ( I\u003Cjats:sub>Na\u003C\u002Fjats:sub>), L-type calcium ( I\u003Cjats:sub>Ca\u003C\u002Fjats:sub>), hyperpolarization-activated pacemaker ( I\u003Cjats:sub>f\u003C\u002Fjats:sub>), transient outward potassium ( I\u003Cjats:sub>to\u003C\u002Fjats:sub>), inward rectifier potassium ( I\u003Cjats:sub>K1\u003C\u002Fjats:sub>), and the rapidly and slowly activating components of delayed rectifier potassium ( I\u003Cjats:sub>Kr\u003C\u002Fjats:sub> and I\u003Cjats:sub>Ks\u003C\u002Fjats:sub>, respectively) current. The high purity and large cell numbers also enabled automated patch-clamp analysis. We conclude that these hiPSC-derived cardiomyocytes have ionic currents and channel gating properties underlying their APs and EADs that are quantitatively similar to those reported for human cardiac myocytes. These hiPSC-derived cardiomyocytes have the added advantage that they can be used in high-throughput assays, and they have the potential to impact multiple areas of cardiovascular research and therapeutic applications. \u003C\u002Fjats:p>","\u003Cjats:p> Tế bào gốc đa năng cảm ứng từ con người (hiPSCs) có khả năng phân hóa thành các tế bào cơ tim chức năng; tuy nhiên, các đặc tính sinh điện học của tế bào cơ tim có nguồn gốc từ hiPSC vẫn chưa được đặc trưng đầy đủ. Chúng tôi đã thực hiện phân tích chi tiết các đặc tính sinh điện học của tế bào cơ tim hiPSC có độ tinh khiết cao. Các tiềm năng hành động (APs) được ghi lại từ các tế bào cơ tim tự phát đập bằng phương pháp patch perforated và có các đặc tính giống như nhĩ, nốt và thất. AP giống như thất phổ biến hơn và có tiềm năng tâm trương cực đại gần giống với các tế bào cơ tim người, thời gian AP nằm trong phạm vi của khoảng QT điện tâm đồ bình thường ở người, và AP cho thấy độ nhạy mong đợi với nhiều loại thuốc (tetrodotoxin, nifedipine và E4031). Các hiện tượng khử cực sớm (EADs) được kích thích bằng E4031 và phụ thuộc vào nhịp tim chậm, và điện áp đỉnh của EAD thay đổi tỷ lệ nghịch với tiềm năng khôi phục của EAD. Các đặc tính điều khiển của bảy dòng ion đã được nghiên cứu bao gồm natri ( I\u003Cjats:sub>Na\u003C\u002Fjats:sub>), canxi loại L ( I\u003Cjats:sub>Ca\u003C\u002Fjats:sub>), máy phát nhịp được kích hoạt bởi siêu phân cực ( I\u003Cjats:sub>f\u003C\u002Fjats:sub>), kali thoáng qua ra ngoài ( I\u003Cjats:sub>to\u003C\u002Fjats:sub>), kali chỉnh lưu vào trong ( I\u003Cjats:sub>K1\u003C\u002Fjats:sub>), và các thành phần hoạt động nhanh và chậm của dòng kali điều chỉnh muộn ( I\u003Cjats:sub>Kr\u003C\u002Fjats:sub> và I\u003Cjats:sub>Ks\u003C\u002Fjats:sub>, tương ứng). Độ tinh khiết cao và số lượng tế bào lớn cũng cho phép phân tích patch-clamp tự động. Chúng tôi kết luận rằng các tế bào cơ tim có nguồn gốc từ hiPSC này có các dòng ion và các đặc tính điều khiển kênh nền tảng cho APs và EADs của chúng tương tự về mặt định lượng với những gì đã được báo cáo cho tế bào cơ tim người. Những tế bào cơ tim có nguồn gốc từ hiPSC này còn có lợi thế bổ sung là chúng có thể được sử dụng trong các thử nghiệm có độ thông lượng cao, và chúng có tiềm năng ảnh hưởng đến nhiều lĩnh vực nghiên cứu tim mạch và ứng dụng điều trị.\u003C\u002Fjats:p>",{"EN":2501,"VI":2502},"High purity human-induced pluripotent stem cell-derived cardiomyocytes: electrophysiological properties of action potentials and ionic currents","Tế bào cơ tim sinh ra từ tế bào gốc đa năng cảm ứng người có độ tinh khiết cao: các đặc tính sinh điện học của các tiềm năng hành động và dòng ion",{"VOID":2504},"21890694",{"VOID":2506},"10.1152\u002Fajpheart.00694.2011",[130],[2043],"https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fajpheart.00694.2011",[2511,2530,2549,2566,2581,2598,2617,2634,2651],{"id":2512,"sortIndex":25,"researcher":24,"roles":2513,"affiliations":2514,"properties":2523,"displayName":2527,"givenName":24,"familyName":24},"78b0361a-31ba-41f8-b802-cba9002c9584",[],[2515],{"id":2516,"sortIndex":25,"affiliation":2517,"properties":24},"5df79629-be0f-45e3-aed9-1bde90a9b886",{"id":2516,"createTime":24,"updateTime":24,"relativeEntities":2518,"slug":24,"properties":2519,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2522,"statistic":24},[],{"title":2520},{"VI":2521},"Cellular Dynamics International, Madison, Wisconsin, USA",[],{"orcid":2524,"title":2526,"openalex":2528},{"VOID":2525},"https:\u002F\u002Forcid.org\u002F0000-0003-3929-6040",{"EN":2527},"Junyi Ma",{"VOID":2529},"A5100686325",{"id":2531,"sortIndex":152,"researcher":24,"roles":2532,"affiliations":2533,"properties":2542,"displayName":2546,"givenName":24,"familyName":24},"9482a609-6271-4b22-9526-94820b8c41fd",[],[2534],{"id":2535,"sortIndex":25,"affiliation":2536,"properties":24},"d157356e-326e-45cf-929b-4398d1de970a",{"id":2535,"createTime":24,"updateTime":24,"relativeEntities":2537,"slug":24,"properties":2538,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2541,"statistic":24},[],{"title":2539},{"VI":2540},"Hoffmann-LaRoche, Nutley, New Jersey",[],{"orcid":2543,"title":2545,"openalex":2547},{"VOID":2544},"https:\u002F\u002Forcid.org\u002F0000-0003-4738-4366",{"EN":2546},"Liang Guo",{"VOID":2548},"A5015228968",{"id":2550,"sortIndex":170,"researcher":24,"roles":2551,"affiliations":2552,"properties":2561,"displayName":2563,"givenName":24,"familyName":24},"975ba2a3-4674-488d-8bcf-57d7d8e5e833",[],[2553],{"id":2554,"sortIndex":25,"affiliation":2555,"properties":24},"3aa82ac4-ae4e-49ea-8ed4-638d4c4da436",{"id":2554,"createTime":24,"updateTime":24,"relativeEntities":2556,"slug":24,"properties":2557,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2560,"statistic":24},[],{"title":2558},{"EN":2559},"Cellular Dynamics International, Madison, Wisconsin; and",[],{"title":2562,"openalex":2564},{"EN":2563},"Steve Fiene",{"VOID":2565},"A5076884143",{"id":2567,"sortIndex":186,"researcher":24,"roles":2568,"affiliations":2569,"properties":2576,"displayName":2578,"givenName":24,"familyName":24},"07890915-faf3-4b1d-895e-6d245b5ac2ea",[],[2570],{"id":2554,"sortIndex":25,"affiliation":2571,"properties":24},{"id":2554,"createTime":24,"updateTime":24,"relativeEntities":2572,"slug":24,"properties":2573,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2575,"statistic":24},[],{"title":2574},{"EN":2559},[],{"title":2577,"openalex":2579},{"EN":2578},"Blake D. 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The novel SARS coronavirus SARS-CoV-2 pandemic may be particularly deleterious to patients with underlying cardiovascular disease (CVD). The mechanism for SARS-CoV-2 infection is the requisite binding of the virus to the membrane-bound form of angiotensin-converting enzyme 2 (ACE2) and internalization of the complex by the host cell. Recognition that ACE2 is the coreceptor for the coronavirus has prompted new therapeutic approaches to block the enzyme or reduce its expression to prevent the cellular entry and SARS-CoV-2 infection in tissues that express ACE2 including lung, heart, kidney, brain, and gut. ACE2, however, is a key enzymatic component of the renin-angiotensin-aldosterone system (RAAS); ACE2 degrades ANG II, a peptide with multiple actions that promote CVD, and generates Ang-(1–7), which antagonizes the effects of ANG II. Moreover, experimental evidence suggests that RAAS blockade by ACE inhibitors, ANG II type 1 receptor antagonists, and mineralocorticoid antagonists, as well as statins, enhance ACE2 which, in part, contributes to the benefit of these regimens. In lieu of the fact that many older patients with hypertension or other CVDs are routinely treated with RAAS blockers and statins, new clinical concerns have developed regarding whether these patients are at greater risk for SARS-CoV-2 infection, whether RAAS and statin therapy should be discontinued, and the potential consequences of RAAS blockade to COVID-19-related pathologies such as acute and chronic respiratory disease. The current perspective critically examines the evidence for ACE2 regulation by RAAS blockade and statins, the cardiovascular benefits of ACE2, and whether ACE2 blockade is a viable approach to attenuate COVID-19. \u003C\u002Fjats:p>\u003Cjats:p> Listen to this article’s corresponding podcast at: https:\u002F\u002Fajpheart.podbean.com\u002Fe\u002Fcovid-19-ace2-and-the-cardiovascular-consequences\u002F . \u003C\u002Fjats:p>","\u003Cjats:p> Đại dịch coronavirus SARS-CoV-2 mới có thể đặc biệt gây hại cho những bệnh nhân có bệnh lý tim mạch nền (CVD). Cơ chế nhiễm SARS-CoV-2 là sự liên kết cần thiết của virus với dạng enzyme chuyển đổi angiotensin 2 (ACE2) gắn trên màng và sự nội hóa phức hợp này vào tế bào chủ. Nhận thức rằng ACE2 là thụ thể đồng cho coronavirus đã thúc đẩy các phương pháp điều trị mới nhằm chặn enzyme này hoặc giảm sự biểu hiện của nó để ngăn chặn sự xâm nhập vào tế bào và nhiễm SARS-CoV-2 vào các tổ chức biểu hiện ACE2 như phổi, tim, thận, não và ruột. Tuy nhiên, ACE2 là một thành phần enzym quan trọng trong hệ thống renin-angiotensin-aldosterone (RAAS); ACE2 phân hủy ANG II, một peptide có nhiều tác dụng thúc đẩy CVD, và tạo ra Ang-(1–7), có tác dụng đối kháng với hiệu ứng của ANG II. Hơn nữa, các bằng chứng thực nghiệm cho thấy việc chặn RAAS bằng các thuốc ức chế ACE, các thuốc đối kháng thụ thể ANG II loại 1, và các thuốc đối kháng mineralocorticoid, cũng như statin, làm tăng ACE2, là một phần trong những lợi ích của các chế độ điều trị này. Với thực tế rằng nhiều bệnh nhân lớn tuổi mắc tăng huyết áp hoặc các bệnh lý tim mạch khác thường xuyên được điều trị bằng các thuốc chặn RAAS và statin, những lo ngại lâm sàng mới đã phát sinh về việc liệu những bệnh nhân này có nguy cơ cao hơn mắc SARS-CoV-2, liệu liệu pháp RAAS và statin có nên ngừng sử dụng, và các hậu quả tiềm tàng của việc chặn RAAS đối với các bệnh lý liên quan đến COVID-19 như bệnh hô hấp cấp và mãn tính. Quan điểm hiện tại sẽ xem xét một cách nghiêm túc các bằng chứng về việc điều chỉnh ACE2 bởi sự chặn RAAS và statin, những lợi ích tim mạch của ACE2, và liệu việc chặn ACE2 có phải là một phương pháp khả thi để giảm thiểu COVID-19 hay không.\u003C\u002Fjats:p>\u003Cjats:p> Nghe podcast liên quan đến bài viết này tại: https:\u002F\u002Fajpheart.podbean.com\u002Fe\u002Fcovid-19-ace2-and-the-cardiovascular-consequences\u002F . \u003C\u002Fjats:p>",{"EN":2923,"VI":2924},"COVID-19, ACE2, and the cardiovascular consequences","COVID-19, ACE2 và những hậu quả về tim mạch",{"VOID":2926},"32228252",{"VOID":2928},"10.1152\u002Fajpheart.00217.2020",[130],[2043],"https:\u002F\u002Fjournals.physiology.org\u002Fdoi\u002F10.1152\u002Fajpheart.00217.2020",[2933,2952,2967],{"id":2934,"sortIndex":25,"researcher":24,"roles":2935,"affiliations":2936,"properties":2945,"displayName":2949,"givenName":24,"familyName":24},"dd38d71d-4e13-4dd5-b5df-a16f8e9dcdb0",[],[2937],{"id":2938,"sortIndex":25,"affiliation":2939,"properties":24},"6bd129c9-3ba3-453d-97f7-7f64096e4256",{"id":2938,"createTime":24,"updateTime":24,"relativeEntities":2940,"slug":24,"properties":2941,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2944,"statistic":24},[],{"title":2942},{"EN":2943},"Cardiovascular Sciences Center, Wake Forest School of Medicine, Winston-Salem, North Carolina",[],{"orcid":2946,"title":2948,"openalex":2950},{"VOID":2947},"https:\u002F\u002Forcid.org\u002F0000-0002-3204-4142",{"EN":2949},"Andrew M. 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