Ferroptosis in the pathogenesis of diabetic cardiomyopathy: mechanisms and therapeutic potential

Diabetic cardiomyopathy (DCM) is a significant complication of diabetes mellitus, often leading to heart failure and increased mortality. While its pathogenesis remains incompletely understood, key contributors include chronic hyperglycemia, hyperlipidemia, insulin resistance, myocardial fibrosis, oxidative stress, mitochondrial dysfunction, and aberrant cell death pathways. Emerging evidence highlights ferroptosis, an iron-dependent form of regulated cell death, as a critical player in DCM progression. This review synthesizes current knowledge on the mechanistic links between ferroptosis and DCM, focusing on endothelial dysfunction, myocardial fibrosis, oxidative stress, and mitochondrial damage. We also discuss promising therapeutic strategies targeting ferroptosis to alleviate DCM, including pharmacological inhibitors, natural compounds, and non-coding RNAs, while identifying gaps for future research.