Antioxidant proteins can be potential targets in ameliorating ferroptosis in diabetic cardiomyopathy: a literature review

Diabetic cardiomyopathy (DCM) is one of the cardiovascular complications of diabetes mellitus, which is different from myocardial damage caused by coronary ischemia, hypertension, and valvular disease. DCM lacks distinct clinical manifestations in its early stages, and current therapeutic approaches primarily focus on symptomatic management. Emerging evidence indicates that even with optimized glycemic regulation, the pathophysiological progression of DCM remains unmitigated. Exploring the pathogenic mechanism of DCM is the focus and hotspot of current research. Ferroptosis, an iron-dependent form of regulatory cell death, is crucial in DCM myocardial damage. Dysfunctional antioxidant defense system, increased oxidative stress, and elevated reactive oxygen species are the key mechanisms of ferroptosis in DCM. Thus, this review innovatively takes antioxidant proteins as the entry point, and for the first time systematically summarizes the molecular mechanism of antioxidant proteins to improve DCM by regulating the ferroptosis pathway, and summarizes the therapeutic strategy of medications to enhance ferroptosis in DCM by targeting the expression of antioxidant proteins, to explore the potential targets to improve ferroptosis in DCM, to provide a new perspective for the study of delaying the progression of DCM.