Cardiovascular diseases (CVDs) remain a leading cause of death worldwide. Mitochondria, essential organelles within cells, play a crucial role in maintaining cardiovascular health by producing energy through ATP synthesis. The heart’s high energy demand makes it particularly sensitive to mitochondrial function. In CVDs, mitochondrial adaptability is compromised, resulting in dysfunction characterized by impaired respiratory chain activity, decreased ATP production, oxidative stress, and structural damage. This review consolidates current research on mitochondrial roles in CVD development, focusing on mitochondrial respiration, ATP synthesis, and the processes involved in maintaining mitochondrial quality, such as mitophagy. It discusses the challenges in developing therapies aimed at restoring mitochondrial function, including drug delivery issues and targeting specificity. The assessment includes analysis of mitochondrial anomalies associated with cardiac disease progression and potential therapeutic strategies. Mitochondrial dysfunction contributes to the progression of various CVDs by reducing energy output and increasing oxidative stress, leading to cardiomyocyte injury and death. Damaged mitochondria produce excessive reactive oxygen species (ROS), exacerbating cellular damage. Repairing mitochondrial components, especially the respiratory chain and ATP synthesis pathways, has shown potential in mitigating cellular injury and improving cardiac function. Restoring mitochondrial function is vital for preventing and treating CVDs. Targeted therapies that repair mitochondrial respiratory activity and enhance ATP production may reduce cellular damage, promote cardiomyocyte survival, and improve clinical outcomes. Understanding mitochondrial dynamics offers promising avenues for innovative interventions in cardiovascular health management.
Manna et al. (Fri,) studied this question.