参考文献/References:
[1] Benjamin EJ,Muntner P,Alonso A,et al. Heart disease and stroke statistics—2019 update:a report from the American Heart Association[J]. Circulation,2019,139(10):e56-e528.
[2] Kubli DA,Gustafsson AB. Mitochondria and mitophagy:the yin and yang of cell death control[J]. Circ Res,2012,111(9):1208-1221.
[3] Bonora M,Wieckowski MR,Sinclair DA,et al. Targeting mitochondria for cardiovascular disorders: therapeutic potential and obstacles[J]. Nat Rev Cardiol,2019,16(1):33-55.
[4] Brown DA,Perry JB,Allen ME,et al. Expert consensus document:mitochondrial function as a therapeutic target in heart failure[J]. Nat Rev Cardiol,2017,14(4):238-250.
[5] Sun N,Finkel T.Cardiac mitochondria:a surprise about size[J]. J Mol Cell Cardiol,2015,82:213-215.
[6] Hoppel CL,Tandler B,Fujioka H,et al. Dynamic organization of mitochondria in human heart and in myocardial disease[J]. Int J Biochem Cell Biol,2009,41(10):1949-1956.
[7] Twig G,Shirihai OS. The interplay between mitochondrial dynamics and mitophagy[J]. Antioxid Redox Signal,2011,14(10):1939-1951.
[8] Hall AR,Hausenloy DJ. The shape of things to come:mitochondrial fusion and fission in the adult heart[J]. Cardiovasc Res,2012,94(3):391-392.
[9] Cipolat S,Martins de BO,Dal ZB,et al. OPA1 requires mitofusin 1 to promote mitochondrial fusion[J]. Proc Natl Acad Sci U S A,2004,101(45):15927-15932.
[10] Kane LA,Lazarou M,Fogel AI,et al. PINK1 phosphorylates ubiquitin to activate Parkin E3 ubiquitin ligase activity[J]. J Cell Biol,2014,205(2):143-153.
[11] 塔娜,梁雨亭,王丹,等. PINK1/Parkin相关线粒体自噬与心血管疾病的研究进展[J]. 心血管病学进展,2019,40(4):601-604.
[12] Lazarou M,Sliter DA,Kane LA,et al. The ubiquitin kinase PINK1 recruits autophagy receptors to induce mitophagy[J]. Nature,2015,524(7565):309-314.
[13] Abdelwahid E,Stulpinas A,Kalvelyte A. Effective agents targeting the mitochondria and apoptosis to protect the heart[J]. Curr Pharm Des,2017,23(8):1153-1166.
[14] Liu YF,Chu YY,Zhang XZ,et al. TGFβ1 protects myocardium from apoptosis and oxidative damage after ischemia reperfusion[J]. Eur Rev Med Pharmacol Sci,2017,21(7):1551-1558.
[15] Bhuiyan MS,Fukunaga K. Activation of HtrA2,a mitochondrial serine protease mediates apoptosis:current knowledge on HtrA2 mediated myocardial ischemia/reperfusion injury[J]. Cardiovasc Ther,2008,26(3):224-232.
[16] Dorn GW 2nd. Mitochondrial pruning by Nix and BNip3:an essential function for cardiac-expressed death factors[J]. J Cardiovasc Transl Res,2010,3(4):374-383 .
[17] Penna C,Mancardi D,Rastaldo R,et al. Cardioprotection:a radical view Free radicals in pre and postconditioning[J]. Biochim Biophys Acta,2009,1787(7):781-793.
[18] Tang X,Luo YX,Chen HZ,et al. Mitochondria, endothelial cell function, and vascular diseases[J]. Front Physiol,2014,5:175.
[19] Mahmod M,Francis JM,Pal N,et al. Myocardial perfusion and oxygenation are impaired during stress in severe aortic stenosis and correlate with impaired energetics and subclinical left ventricular dysfunction[J]. J Cardiovasc Magn Reson,2014,16:29.
[20] Maslov MY,Chacko VP,Hirsch GA,et al. Reduced in vivo high-energy phosphates precede adriamycin-induced cardiac dysfunction[J]. Am J Physiol Heart Circ Physiol,2010,299(2):H332-H337
[21] Ashrafian H. Cardiac energetics in congestive heart failure[J]. Circulation,2002,105(6):e44-e45.
[22] Angelova PR,Abramov AY. Functional role of mitochondrial reactive oxygen species in physiology[J]. Free Radic Biol Med,2016,100:81-85.
[23] Watanabe T,Saotome M,Nobuhara M,et al. Roles of mitochondrial fragmentation and reactive oxygen species in mitochondrial dysfunction and myocardial insulin resistance[J]. Exp Cell Res,2014,323(2):314-325.
[24] Salabei JK,Hill BG. Mitochondrial fission induced by platelet-derived growth factor regulates vascular smooth muscle cell bioenergetics and cell proliferation[J]. Redox Biol,2013,1:542-551.
[25] Gustafsson AB,Gottlieb RA.Autophagy in ischemic heart disease[J]. Circ Res,2009,104(2):150-158.
[26] Disatnik MH,Ferreira JC,Campos JC,et al. Acute inhibition of excessive mitochondrial fission after myocardial infarction prevents long-term cardiac dysfunction[J]. J Am Heart Assoc,2013,2(5):e000461.
[27] Wijnker PJM,Sequeira V,Kuster DWD,et al. Hypertrophic cardiomyopathy:a vicious cycle triggered by sarcomere mutations and secondary disease hits[J]. Antioxid Redox Signal,2019,31(4):318-358.
[28] Brown DI,Griendling KK. Regulation of signal transduction by reactive oxygen species in the cardiovascular system[J]. Circ Res,2015,116(3):531-549.
[29] Goffart S,von Kleist-Retzow JC,Wiesner RJ. Regulation of mitochondrial proliferation in the heart:power-plant failure contributes to cardiac failure in hypertrophy[J]. Cardiovasc Res,2004,64(2):198-207.
[30] Pennanen C,Parra V,López-Crisosto C,et al. Mitochondrial fission is required for cardiomyocyte hypertrophy mediated by a Ca2+-calcineurin signaling pathway[J]. J Cell Sci,2014,127(Pt 12):2659-2671.
[31] Weiss JN,Garfinkel A,Karagueuzian HS,et al. Early afterdepolarizations and cardiac arrhythmias[J]. Heart Rhythm,2010,7(12):1891-1899.
[32] Aggarwal NT,Makielski JC. Redox control of cardiac excitability[J]. Antioxid Redox Signal,2013,18(4):432-468.
[33] Karam BS,Chavez-Moreno A,Koh W,et al. Oxidative stress and inflammation as central mediators of atrial fibrillation in obesity and diabetes[J]. Cardiovasc Diabetol,2017,16(1):120.
[34] Sommese L,Valverde CA,Blanco P,et al. Ryanodine receptor phosphorylation by CaMKⅡpromotes spontaneous Ca(2+) release events in a rodent model of early stage diabetes:the arrhythmogenic substrate[J]. Int J Cardiol,2016,202:394-406.
[35] LaRocca TJ,Fabris F,Chen J,et al. Na+/Ca2+ exchanger-1 protects against systolic failure in the Akitains2 model of diabetic cardiomyopathy via a CXCR4/NF- κB pathway[J]. Am J Physiol Heart Circ Physiol,2012,303(3):H353-H367.
[36] Liu M,Liu H,Dudley SC Jr. Reactive oxygen species originating from mitochondria regulate the cardiac sodium channel[J]. Circ Res,2010,107(8):967-974.
[37] Mesubi OO,Anderson ME. Atrial remodelling in atrial fibrillation:CaMKII as a nodal proarrhythmic signal[J]. Cardiovasc Res,2016,109(4):542-557.
[38] Yang R,Ernst P,Song J,et al. Mitochondrial-mediated oxidative Ca2+/calmodulin-dependent kinaseⅡactivation induces early afterdepolarizations in guinea pig cardiomyocytes:an in silico study[J]. J Am Heart Assoc,2018,7(15):e008939.
相似文献/References:
[1]李开 饶莉.线粒体自噬的分子生物学过程及其在心脏疾病中的作用[J].心血管病学进展,2022,(3):222.[doi:10.16806/j.cnki.issn.1004-3934.2022.03.000]
LI Kai,RAO Li.Molecular Biological Process of Mitophagy and Its Role in Heart Diseases[J].Advances in Cardiovascular Diseases,2022,(3):222.[doi:10.16806/j.cnki.issn.1004-3934.2022.03.000]
[2]程晓蔚 朱庆磊.线粒体ATP敏感钾通道线粒体自噬对心力衰竭的作用研究[J].心血管病学进展,2023,(2):163.[doi:10.16806/j.cnki.issn.1004-3934.2023.02.015]
CHENG XiaoweiZHU Qinglei.The Role of Mitochondrial ATP-Sensitive Potassium Channel[J].Advances in Cardiovascular Diseases,2023,(3):163.[doi:10.16806/j.cnki.issn.1004-3934.2023.02.015]
[3]李心瑶 陈俊 李灼.脓毒症心肌病的发病机制研究进展[J].心血管病学进展,2024,(1):44.[doi:10.16806/j.cnki.issn.1004-3934.2023.01.012]
LI Xinyao,CHEN Jun,LI Zhuo.Pathogenesis of Septic Cardiomyopathy[J].Advances in Cardiovascular Diseases,2024,(3):44.[doi:10.16806/j.cnki.issn.1004-3934.2023.01.012]
[4]丁姝颖 于子翔 马依彤.线粒体功能障碍与血管钙化发生的研究进展[J].心血管病学进展,2024,(3):253.[doi:10.16806/j.cnki.issn.1004-3934.2024.03.014]
DING Shuying,YU Zixiang,MA Yitong.Research Progress in Mitochondria Dysfunction and the Development of Vascular Calcification[J].Advances in Cardiovascular Diseases,2024,(3):253.[doi:10.16806/j.cnki.issn.1004-3934.2024.03.014]
[5]王璐 桑婉玥 简易 韩亚凡 王菲菲 李耀东.抑制MAPK14通过减轻线粒体自噬改善AngⅡ诱导的心房颤动[J].心血管病学进展,2024,(4):373.[doi:10.16806/j.cnki.issn.1004-3934.2024.04.019]
WANG Lu,SANG Wanyue,JIAN Yi,et al.Inhibition of MAPK14 Improves Ang-Induced Atrial Fibrillation by Reducing Mitochondrial Autophagy[J].Advances in Cardiovascular Diseases,2024,(3):373.[doi:10.16806/j.cnki.issn.1004-3934.2024.04.019]
[6]鄢文婷 黄愿 王刚 李燕玲 谢萍.线粒体功能障碍与放射性心脏损伤的研究进展[J].心血管病学进展,2024,(6):557.[doi:10.16806/j.cnki.issn.1004-3934.2024.06.018]
YAN Wenting,HUANG Yuan,WANG Gang,et al.Mitochondrial Dysfunction and Radiation -Induced Heart Disease[J].Advances in Cardiovascular Diseases,2024,(3):557.[doi:10.16806/j.cnki.issn.1004-3934.2024.06.018]