Mitochondria generate ATP to support energy-dependent reactions in the cells, they also integrate redox signaling to regulate cell death, proliferation, and autophagy pathways. Although protein machineries for processes such as oxidative phosphorylation and tricarboxylic cycle (TCA) were identified for decades, emerging studies have begun to appreciate the regulatory mechanisms of mitochondrial function by mitochondrial DNA (mtDNA) maintenance, mitochondrial dynamics, and posttranslational modifications of mitochondrial proteins. Oxidative stress has long been suggested to be one of the driving forces of disease and aging, and mitochondria are both the major source and targets of reactive oxygen species. Dysfunction of the regulatory mechanisms could result in oxidative stress and amplify ischemia/reperfusion injury, which leads to the pathogenesis of cardiovascular diseases, such as cardiac infarction, myocardial fibrosis, hypertrophy and heart failure. Filling the knowledge gap in the interplay between oxidative stress and mitochondrial function in cardiovascular pathologies could lead to potential therapeutic strategies targeting mitochondrial dysfunction.

We invite investigators to contribute original research articles as well as reviews concerning advances in the causal relationships of mitochondrial dysfunction and oxidative stress in the progression of cardiovascular diseases. We encourage the submission of original studies and reviews, both clinical and scientific, describing the pathophysiological mechanisms, prevention, and treatment, on all aspects of cardiovascular medicine (such as heart failure, ischemic heart disease, disease or injury related to cardiac surgery).

Potential topics include but are not limited to the following:

• The interplay between mitochondrial function and oxidative stress in cardiovascular pathophysiology
• Role of metabolic disorders in oxidative cardiomyopathy
• Impact of protein posttranslational modifications in oxidative stress and cardiomyopathy
• Inter-organelle crosstalk and myocardial redox signaling
• Transcriptional regulation of oxidative/antioxidative genes in cardiac diseases
• Oxidative stress and myocardial inflammation
• Pathophysiological consequences and contribution of oxidative stress to heart failure
• The effects of mitochondrial DNA maintenance, mitochondrial dynamics, and mitochondrial protein quality control on myocardial oxidative stress
• Potential antioxidative approaches and molecular mechanisms in the treatment of cardiovascular diseases, such as HFpEF and adverse outcomes from COVID19 infection
• Latest developments in NAD -based cardiovascular therapeutics