Electron transport chain dysfunction in neonatal pressure-overload hypertrophy precedes cardiomyocyte apoptosis independent of oxidative stress
- 30 June 2010
- journal article
- Published by Elsevier BV in The Journal of Thoracic and Cardiovascular Surgery
- Vol. 139 (6), 1609-1617
- https://doi.org/10.1016/j.jtcvs.2009.08.060
Abstract
No abstract availableKeywords
This publication has 42 references indexed in Scilit:
- Myocyte apoptosis occurs early during the development of pressure-overload hypertrophy in infant myocardiumThe Journal of Thoracic and Cardiovascular Surgery, 2009
- Domestication of the cardiac mitochondrion for energy conversionJournal of Molecular and Cellular Cardiology, 2009
- Energy metabolism in heart failure and remodellingCardiovascular Research, 2008
- Cytochrome c oxidase biogenesis: New levels of regulationIUBMB Life, 2008
- Mitochondrial Oxidative Stress, DNA Damage, and Heart FailureAntioxidants and Redox Signaling, 2006
- Vascular Endothelial Growth Factor Prevents Apoptosis and Preserves Contractile Function in Hypertrophied Infant HeartCirculation, 2006
- Activation of Mitogen-Activated Protein Kinases by Lysophosphatidylcholine-Induced Mitochondrial Reactive Oxygen Species Generation in Endothelial CellsThe American Journal of Pathology, 2006
- Hypoxia-Inducible Factor 1-Alpha Reduces Infarction and Attenuates Progression of Cardiac Dysfunction After Myocardial Infarction in the MouseJournal of the American College of Cardiology, 2005
- Role of mitochondria in human agingJournal of Biomedical Science, 1997
- An Evaluation of the Measurement of the Activities of Complexes I-IV in the Respiratory Chain of Human Skeletal Muscle MitochondriaBiochemical Medicine and Metabolic Biology, 1994