Mitochondrial Damage and Dysfunction in Cardiovascular Disease

Dear Colleagues,

Mitochondria provide the cell’s energy through the electron transport chain and oxidative phosphorylation. Maintaining a highly efficient energy production (bioenergetics) is critical for the optimal functions of the cardiac tissues. Abnormalities in bioenergetics can compromise the cardiac tissues, leading to less efficient cardiomyocytes. These changes in energy metabolism are associated with many diseases, including heart failure, cardiomyopathies, and other cardiovascular diseases (CVD). Besides energy production, the mitochondria play a significant role in maintaining the homeostasis of cellular cations by regulating Ca²⁺, K⁺, and Na⁺ ions which are critical for electrical activity and muscle contraction. Abnormalities in the mitochondria inner membrane ion channels can result in dysfunction that contributes to CVD.

The maternally inherited, circular mitochondrial (mt) DNA is susceptible to oxidative damage but, unlike nuclear DNA, it cannot be effectively repaired. Therefore, mtDNA damage can accumulate and contribute to cardiac diseases. As mitochondrial bioenergetics declines, cells can produce higher levels of reactive oxygen species (ROS) that damage proteins, lipids, and DNA, thereby leading to increased apoptosis, autophagy, and mitophagy. In CVD, mitochondrial dysfunction and oxidative stress can be associated with damage to cardiomyocytes, cardiac vessels, and cardiac electrical functioning. Many of these deleterious cardiac events can be accelerated by comorbidities such as diabetes. Investigations into mitochondria-targeting drugs and/or mitochondria replacement therapies are cautiously being pursued.

This Special Issue aims to highlight the importance of mitochondrial bioenergetics, the deleterious effects of mtDNA damage, and possible future therapeutic approaches for the rescue of mitochondria dysfunction in cardiovascular diseases. Making mitochondria the central focus in complex, multifactorial cardiovascular diseases may lead to novel therapies improving patients’ outcomes.

We look forward to your expert contributions.

Dr. Sonali Nashine
Prof. Dr. Maria Cristina Kenney
Guest Editors

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• mitochondria
• cardiovascular disease
• bioenergetics
• mitochondrial genetics
• apoptosis
• therapuetics