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已发表论文
铁死亡：心血管疾病发病机制与治疗的关键环节
Authors Guo S, Liu J, Hua J, Ding L, Chen Q
Received 13 November 2025
Accepted for publication 3 December 2025
Published 19 December 2025 Volume 2025:18 Pages 7675—7697
DOI https://doi.org/10.2147/IJGM.S581227
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 4
Editor who approved publication: Dr Redoy Ranjan
Shuxian Guo,* Jie Liu,* Juan Hua, Lan Ding, Qi Chen
Department of Cardiovascular Medicine, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Qi Chen, Department of Cardiovascular Medicine, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, People’s Republic of China, Tel +86 13330087693, Email efycq@189.cn
Abstract: In the pathogenesis of cardiovascular diseases (CVDs), ferroptosis is increasingly implicated as a key mechanism. This iron-driven, regulated cell death is characterized by the accumulation of lipid peroxides and a deficiency in glutathione. This comprehensive review delineates the molecular underpinnings of ferroptosis—encompassing dysregulated iron metabolism, GPX4 inactivation, and lipid peroxidation—and elucidates its pivotal role in a spectrum of cardiac pathologies. Notably, ferroptosis contributes to oxidative stress, mitochondrial dysfunction, and inflammatory responses, accelerating myocardial damage and functional decline. Emerging evidence indicates that several drugs targeting the ferroptosis pathway including iron chelators, antioxidants, and small-molecule inhibitors such as ferrostatin-1 and liproxstatin-1, demonstrate cardioprotective effects in preclinical models. However, translational challenges remain, including context-dependent roles of regulators like p53 and AMPK, and the need for organelle-specific interventions. This review synthesizes current knowledge and proposes ferroptosis as a promising target for precision medicine in CVDs, urging further research into biomarkers and combination therapies to mitigate the global burden of cardiovascular morbidity and mortality.
Keywords: ferroptosis, cardiovascular diseases, reactive oxygen species, lipid peroxidation, pathogenesis, therapy
Department of Cardiovascular Medicine, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Qi Chen, Department of Cardiovascular Medicine, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, People’s Republic of China, Tel +86 13330087693, Email efycq@189.cn
Abstract: In the pathogenesis of cardiovascular diseases (CVDs), ferroptosis is increasingly implicated as a key mechanism. This iron-driven, regulated cell death is characterized by the accumulation of lipid peroxides and a deficiency in glutathione. This comprehensive review delineates the molecular underpinnings of ferroptosis—encompassing dysregulated iron metabolism, GPX4 inactivation, and lipid peroxidation—and elucidates its pivotal role in a spectrum of cardiac pathologies. Notably, ferroptosis contributes to oxidative stress, mitochondrial dysfunction, and inflammatory responses, accelerating myocardial damage and functional decline. Emerging evidence indicates that several drugs targeting the ferroptosis pathway including iron chelators, antioxidants, and small-molecule inhibitors such as ferrostatin-1 and liproxstatin-1, demonstrate cardioprotective effects in preclinical models. However, translational challenges remain, including context-dependent roles of regulators like p53 and AMPK, and the need for organelle-specific interventions. This review synthesizes current knowledge and proposes ferroptosis as a promising target for precision medicine in CVDs, urging further research into biomarkers and combination therapies to mitigate the global burden of cardiovascular morbidity and mortality.
Keywords: ferroptosis, cardiovascular diseases, reactive oxygen species, lipid peroxidation, pathogenesis, therapy