Abstract
Diabetic cardiomyopathy (DCM) is a common complication of diabetes, and its pathogenesis remains elusive. Ferroptosis, a process dependent on iron-mediated cell death, plays a crucial role in DCM via disrupted iron metabolism, lipid peroxidation, and weakened antioxidant defenses. Hyperglycemia, oxidative stress, and inflammation may exacerbate ferroptosis in diabetes. This review emphasizes the interaction between cardiac fibroblasts and cardiomyocytes in DCM, influencing ferroptosis occurrence. By exploring ferroptosis modulation for potential therapeutic targets, this article offers a fresh perspective on DCM treatment. The study systematically covers the interplay, mechanisms, and targeted drugs linked to ferroptosis in DCM development.