Oxidative stress and ferroptosis in diabetic cardiomyopathy: mechanistic interplay and therapeutic implications.

Abstract

Diabetic cardiomyopathy (DCM) is a severe cardiovascular complication of diabetes mellitus, characterized by pathological changes such as cardiomyocyte hypertrophy, necrosis, and myocardial fibrosis, which can ultimately lead to heart failure. However, its underlying mechanisms remain incompletely understood, limiting the development of effective therapeutic approaches. In recent years, the critical roles of oxidative stress and ferroptosis in the pathogenesis of DCM have attracted increasing attention. Oxidative stress is a state where the imbalance between oxidative and antioxidant systems results in excessive production of reactive oxygen species (ROS), thereby damaging key cellular structures such as cardiomyocyte membranes and mitochondria, and promoting the occurrence and development of DCM. Ferroptosis is an iron-dependent form of regulated cell death, which has been confirmed to be involved in the injury and death of diabetic cardiomyocytes.This article reviews the interaction between oxidative stress and ferroptosis in DCM as well as their molecular mechanisms, explores their complex relationship in the occurrence and progression of the disease, and proposes potential therapeutic strategies based on this mechanistic framework. It aims to provide researchers and clinicians with a comprehensive and up-to-date reference to collectively advance the prevention and treatment of DCM.