Cross-regulation of methylation and oxidative stress: molecular mechanisms and intervention strategies of diabetic cardiomyopathy.

Diabetic cardiomyopathy (DCM)-a myocardial pathology that is both singular and independent of coronary artery disease and hypertension-constitutes an intrinsically specific cardiac alteration in individuals with diabetes mellitus, whose labyrinthine pathogenesis portends profound compromise of ventricular performance and existential quality of life. In recent years, studies have found that DNA methylation and oxidative stress are closely related to the occurrence and development of diabetic cardiomyopathy. DNA methylation participates in the oxidative damage, metabolic abnormalities, and apoptosis of myocardial cells by regulating the expression of key antioxidant enzymes, inflammatory factors, and mitochondrial function-related genes. Oxidative stress can alter the methylation profile of myocardial cells and exacerbate pathological conditions by activating mechanisms such as DNA methyltransferase. The interaction between the two constitutes an important molecular regulatory axis in diabetes cardiomyopathy. Centering on the intersecting mechanisms of DNA methylation and oxidative stress in diabetic cardiomyopathy, this review dissects their concerted roles in suppressing antioxidant enzyme expression, derailing mitochondrial function, igniting inflammatory cascades, and precipitating cardiomyocyte apoptosis, while systematically enumerating current intervention strategies targeting these pathways-spanning natural products, epigenetic modulators, and antioxidant therapies-with the overarching objective of furnishing both theoretical scaffolding and translational reference for mechanistic inquiry and precision therapeutics in diabetic cardiomyopathy.