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Potential Significance of Targeting Ferroptosis for Intervention of Diabetic Cardiomyopathy
Potential Significance of Targeting Ferroptosis for Intervention of Diabetic Cardiomyopathy
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Potential Significance of Targeting Ferroptosis for Intervention of Diabetic Cardiomyopathy
Potential Significance of Targeting Ferroptosis for Intervention of Diabetic Cardiomyopathy

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Potential Significance of Targeting Ferroptosis for Intervention of Diabetic Cardiomyopathy
Potential Significance of Targeting Ferroptosis for Intervention of Diabetic Cardiomyopathy
Journal Article

Potential Significance of Targeting Ferroptosis for Intervention of Diabetic Cardiomyopathy

2025
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Overview
ABSTRACT Background Diabetes represents a significant global health concern, with diabetic cardiomyopathy (DCM) emerging as a primary cause of mortality among individuals with diabetes. Despite the prevalence of DCM, advancements in therapeutic and preventative strategies remain constrained. Methods Recent studies were reviewed to provide a comprehensive summary of pathogenesis and clinical treatment of DCM, effect of ferroptosis, and potential value of ferroptosis inhibitors in DCM intervention. Results A growing body of research indicates that oxidative stress, inflammatory reactions, and other factors play a role in the onset and progression of DCM. Oxidative stress within cardiomyocytes is a primary mechanism implicated in the development of DCM, whereby heightened intracellular reactive oxygen species (ROS) facilitate cell death via ferroptosis. Ferroptosis inhibitors hold great promise as therapeutic agents. Conclusions This review provides an overview of the involvement of iron homeostasis regulation, oxidative stress, and ferroptosis in DCM, and the significance of ferroptosis in the prevention and treatment of DCM. The pathophysiology of DCM encompasses insulin resistance and hyperglycemia‐induced metabolic alterations in cardiomyocytes, mitochondrial dysfunction and oxidative stress, cardiac lipotoxicity, dysregulation of immune responses, endoplasmic reticulum (ER) stress, impaired calcium handling, and activation of the renin‐angiotensin‐aldosterone system (RAAS). Oxidative stress results in cardiomyocyte hypertrophy, myocardial fibrosis, cardiomyocyte ferroptosis and immune property modulation and ultimately lead to HFpEF. Ferroptosis inhibitors hold great promise as therapeutic agents for the intervention of DCM.