Journal Article Review Epublish
PubMed: 40564057 DOI: 10.3390/biomedicines13061338
Involvement of Oxidative Stress in Mitochondrial Abnormalities During the Development of Heart Disease.
Biomedicines 13(6)
Authors: Naranjan S Dhalla, Petr Ostadal, Paramjit S Tappia
Affiliations
- St. Boniface Hospital Albrechtsen Research Centre, Institute of Cardiovascular Sciences, Department of Physiology & Pathophysiology, Max Rady College of Medicine, University of Manitoba, Winnipeg, MB R2H 2A6, Canada.
- Department of Cardiology, 2nd Faculty of Medicine, Charles University, Motol University Hospital, V Uvalu 84, 15000 Prague, Czech Republic.
- Asper Clinical Research Institute, St. Boniface Hospital, Winnipeg, MB R2H 2A6, Canada.
Abstract
Background: Several mitochondrial abnormalities such as defective energy production, depletion of energy stores, Ca 2+ accumulation, generation of reactive oxygen species, and impaired intracellular signaling are associated with cardiac dysfunction during the development of different heart diseases. Methods: A narrative review was compiled by a search for applicable literature in MEDLINE via PubMed. Results: Mitochondria generate ATP through the processes of electron transport and oxidative phosphorylation, which is used as energy for cardiac contractile function. Mitochondria, in fact, are the key subcellular organelle for the regulation of intracellular Ca 2+ concentration and are considered to serve as a buffer to maintain Ca 2+ homeostasis in cardiomyocytes. However, during the development of heart disease, the excessive accumulation of intracellular Ca 2+ results in mitochondria Ca 2+-overload, which, in turn, impairs mitochondrial energy production and induces cardiac dysfunction. Mitochondria also generate reactive oxygen species (ROS), including superoxide anion radicals and hydroxyl radicals as well as non-radical oxidants such as hydrogen peroxide, which promote lipid peroxidation and the subsequent disturbance of Ca 2+ homeostasis, cellular damage, and death. Conclusion: These observations support the view that both oxidative stress and intracellular Ca 2+-overload play a critical role in mitochondrial disruption during the pathogenesis of different cardiac pathologies.
MeSH
Heart Diseases, Peroxides, Homeostasis, Heart, Stress, Physiological, Mitochondria, Oxidative Stress, Superoxides, Cell Death