Hearts deficient in both Mfn1 and Mfn2 are protected against acute myocardial infarction

• المؤلفون الرئيسيون: Hall, A.R, Burke, N, Dongworth, R.K, Kalkhoran, S.B, Dyson, A, Vicencio, J.M, Dorn, G.W, Yellon, D.M, Hausenloy, D.J
• مؤلفون آخرون: DUKE-NUS MEDICAL SCHOOL
• التنسيق: مقال
• منشور في: Nature Publishing Group 2020
• الموضوعات: antimycin A1; calcium ion; cytochrome c oxidase; mitofusin 1; mitofusin 2; reactive oxygen metabolite; reduced nicotinamide adenine dinucleotide dehydrogenase (ubiquinone); succinate dehydrogenase (ubiquinone); ubiquinol cytochrome c reductase; calcium; carrier protein; guanosine triphosphatase; Mfn1 protein, mouse; Mfn2 protein, mouse; mitochondrial permeability transition pore; acute heart infarction; animal experiment; animal model; Article; cell organelle; confocal microscopy; controlled study; disorders of mitochondrial functions; echocardiography; fractional shortening; heart infarction size; heart left ventricle hypertrophy; heart mitochondrion; heart output; heart protection; mitochondrion swelling; myocardial ischemia reperfusion injury; nonhuman; priority journal; protein expression; animal; cardiac muscle; cardiac muscle cell; deficiency; drug effects; gene expression; genetics; knockout mouse; metabolism; mitochondrial dynamics; mitochondrion; mouse; Myocardial Infarction; Myocardial Reperfusion Injury; pathology; sarcoplasmic reticulum; ultrastructure; Animals; Antimycin A; Calcium; Gene Expression; GTP Phosphohydrolases; Mice; Mice, Knockout; Mitochondria; Mitochondrial Dynamics; Mitochondrial Membrane Transport Proteins; Myocardium; Myocytes, Cardiac; Reactive Oxygen Species; Sarcoplasmic Reticulum
• الوصول للمادة أونلاين: https://scholarbank.nus.edu.sg/handle/10635/180381

10.1038/cddis.2016.139