The Role of Epigenetics in Myocardial Infarction: Mechanism and Therapeutic Potential

The Role of Epigenetics in Myocardial Infarction

Abstract

Myocardial infarction (MI), remains one of the leading causes of morbidity and mortality worldwide. As a result, understanding the underlying mechanisms of MI is crucial for developing effective therapeutic strategies. Epigenetics, which involves heritable changes in gene expression without altering the underlying DNA sequence, has emerged as a significant factor in the pathogenesis and progression of MI. Key epigenetic mechanisms such as DNA methylation, histone modifications, and noncoding RNAs (ncRNAs) have been shown to regulate genes associated with inflammation, apoptosis, fibrosis, and cardiac repair. These epigenetic alterations contribute to the complex gene-environment interactions that influence clinical outcomes in MI patients. Recent research has identified specific epigenetic changes that can serve as biomarkers for MI risk stratification, offering potential for early diagnosis and personalized therapeutic interventions. Moreover, targeting these epigenetic modifications holds promise as a therapeutic strategy to reduce myocardial damage, enhance cardiac function, and prevent adverse remodeling after MI. This review explores the mechanisms by which epigenetic regulation influences MI pathogenesis and discusses the therapeutic potential of targeting these pathways to improve patient outcomes. By integrating epigenetic therapies into clinical practice, it may be possible to revolutionize the treatment of MI, addressing the disease at its molecular roots and offering more effective, durable interventions.