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Research progress on the role and mechanism of ferroptosis in heart diseases

CUI Yu-Tong¹, ZHU Xin-Xin¹, ZHANG Qi¹, QU Ai-Juan^1,2,3,*

¹Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, China；²Key Laboratory of Remodeling-Related Cardiovascular Diseases, Ministry of Education, Beijing 100069, China；³Beijing Key Laboratory of Metabolic Disorder-Related Cardiovascular Diseases, Beijing 100069, Chin

Abstract

Cardiovascular disease remains the leading cause of death in China, with its morbidity and mortality continue to rise. Ferroptosis, a unique form of iron-dependent cell death, plays a major role in many heart diseases. The classical mechanisms of ferroptosis include iron metabolism disorder, oxidative antioxidant imbalance and lipid peroxidation. Recent studies have found many additional mechanisms of ferroptosis, such as coenzyme Q10, ferritinophagy, lipid autophagy, mitochondrial metabolism disorder, and the regulation by nuclear factor erythroid 2-related factor 2 (NRF2). This article reviews recent advances in understanding the mechanisms of ferroptosis and its role in heart failure, myocardial ischemia/reperfusion injury, diabetic cardiomyopathy, myocardial toxicity of doxorubicin, septic cardiomyopathy, and arrhythmia. Furthermore, we discuss the potential of ferroptosis inhibitors/inducers as therapeutic targets for heart diseases, suggesting that ferroptosis may be an important intervention target of heart diseases.

Key words: heart diseases; ferroptosis; ferroptosis inhibitors

Received: 　　Accepted:

Corresponding author: 曲爱娟　　E-mail:

DOI: 10.13294/j.aps.2025.0010

Citing This Article：

CUI Yu-Tong, ZHU Xin-Xin, ZHANG Qi, QU Ai-Juan. Research progress on the role and mechanism of ferroptosis in heart diseases. Acta Physiol Sin 2025; 77 (1): 75-84 (in Chinese with English abstract).