Mitochondrial Dysfunction in Cardiac Diseases: Insights into Pathophysiology and Clinical Outcomes.

Abstract

Mitochondrial dysfunction plays a crucial role in the pathogenesis of various cardiac diseases, including heart failure, ischemic cardiomyopathy, and drug-induced cardiotoxicity. Mitochondria are essential for cellular energy production, calcium homeostasis, redox balance, and apoptotic regulation, making their proper function vital for cardiac health. Dysfunctional mitochondria contribute to excessive reactive oxygen species (ROS) production, impaired ATP synthesis, and disruption of mitochondrial dynamics, leading to cardiomyocyte damage and cell death. Emerging research highlights mitochondrial dynamics, including fission, fusion, mitophagy, and biogenesis, as critical determinants of cardiac homeostasis. Perturbations in these processes exacerbate myocardial injury and heart failure progression. Additionally, chemotherapy-induced cardiotoxicity, primarily from anthracyclines, is closely linked to mitochondrial damage, underscoring the need for targeted therapeutic strategies. Pharmacological interventions, such as antioxidants, mitochondrial-targeted drugs, and cardioprotective agents, have shown promise in mitigating mitochondrial dysfunction-related cardiac toxicity. Furthermore, lifestyle modifications, including exercise and dietary interventions, are being explored to enhance mitochondrial resilience in cardiac tissues. Advanced imaging techniques and biomarker-based diagnostics are improving the early detection of mitochondrial dysfunction in cardiac diseases. Emerging therapeutic strategies, such as mitochondrial transplantation, gene therapy, and precision medicine approaches, hold potential for targeted intervention. Despite these advances, challenges remain in translating mitochondrial-targeted therapies into clinical practice due to complexities in mitochondrial regulation and inter-organ communication. Future research should focus on optimizing mitochondrial-targeted interventions, improving diagnostic precision, and exploring novel molecular pathways to mitigate cardiac mitochondrial dysfunction. A comprehensive understanding of mitochondrial pathophysiology in cardiac diseases will pave the way for innovative treatment strategies aimed at preserving cardiac function and reducing the burden of heart failure.