Ferroptosis: A novel therapeutic target for diabetic cardiomyopathy

Abstract

Ferroptosis is a new type of programmed cell death caused by the accumulation of iron-dependent lipid peroxides, and it plays a role in the occurrence and progression of diverse diseases. Diabetic cardiomyopathy (DCM), a serious cardiovascular complication in patients with diabetes, eventually progresses to refractory heart failure (HF), which increases the risk of hospitalization for HF and cardiovascular death in patients with diabetes. Despite glycemic control, effective strategies to prevent DCM onset are currently lacking. Accumulating evidence suggests that ferroptosis is involved in oxidative stress, inflammation, and abnormal autophagy in diabetic myocardium, which plays an important role in myocardial apoptosis, hypertrophy, and cardiac fibrosis. The inhibition of ferroptosis can relieve DCM. Presently, ferroptosis inhibitors have been broadly suggested for the treatment of iron overload-related cardiomyopathy. This article reviewed relevant studies to offer a new therapeutic target for DCM.

Keywords: Diabetic cardiomyopathy; Ferroptosis; Oxidative stress; Inflammation; Autophagy

Core Tip: Ferroptosis, a form of iron-dependent programmed cell death, plays a key role in the development of diabetic cardiomyopathy (DCM), contributing to oxidative stress, inflammation, and myocardial damage. Inhibiting ferroptosis can potentially alleviate DCM and prevent its progression to heart failure. This emerging pathway offers a promising therapeutic target for DCM, providing new hope for the management of DCM.