DNA methylation regulates key pathophysiological processes including inflammation, autophagy, fibrosis, and cardiomyocyte proliferation after myocardial infarction, highlighting its potential as a therapeutic target.
Myocardial infarction (MI) imposes a huge medical and economic burden on society, and cardiac repair after MI involves a complex series of processes. Understanding the key mechanisms (such as apoptosis, autophagy, inflammation, and fibrosis) will facilitate further drug development and patient treatment. Presently, a substantial body of evidence suggests that the regulation of epigenetic processes contributes to cardiac repair following MI, with DNA methylation being among the notable epigenetic factors involved. This article will review the research on the mechanism of DNA methylation regulation after MI to provide some insights for future research and development of related drugs.
Han et al. (Tue,) conducted a review in Myocardial infarction. DNA methylation regulates key pathophysiological processes including inflammation, autophagy, fibrosis, and cardiomyocyte proliferation after myocardial infarction, highlighting its potential as a therapeutic target.