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REVIEW article

Front. Pharmacol.
Sec. Cardiovascular and Smooth Muscle Pharmacology
Volume 15 - 2024 | doi: 10.3389/fphar.2024.1482986

Ferroptosis and Myocardial Ischemia-Reperfusion: Mechanistic Insights and New Therapeutic Perspectives

Provisionally accepted
Binwei Jin Binwei Jin 1,2,3*Zhiming Zhang Zhiming Zhang 1,2,3*Yang Zhang Yang Zhang 1,2,3*Minjun Yang Minjun Yang 1,2,3*Cheng Wang Cheng Wang 1,2,3*Jiayi Xu Jiayi Xu 1,2,3*Yu Zhu Yu Zhu 1,2,3*Jianjun Jiang Jianjun Jiang 1,2,3*Yafei Mi Yafei Mi 1,2,3*Zhenzhu Sun Zhenzhu Sun 1,2,3*
  • 1 Department of Cardiology, Zhejiang Taizhou Hospital, Taizhou, China
  • 2 Department of Cardiology, Taizhou Hospital, Wenzhou Medical University, Linhai, Zhejiang Province, China
  • 3 Zhejiang Taizhou Hospital, Taizhou, Zhejiang Province, China

The final, formatted version of the article will be published soon.

    Myocardial ischemia-reperfusion injury (MIRI) is a significant factor in the development of cardiac dysfunction following a myocardial infarction. Ferroptosis, a type of regulated cell death driven by iron and marked by lipid peroxidation, has garnered growing interest for its crucial involvement in the pathogenesis of MIRI.This review comprehensively examines the mechanisms of ferroptosis, focusing on its regulation through iron metabolism, lipid peroxidation, VDAC signaling, and antioxidant system dysregulation. We also compare ferroptosis with other forms of cell death to highlight its distinct characteristics. Furthermore, the involvement of ferroptosis in MIRI is examined with a focus on recent discoveries concerning ROS generation, mitochondrial impairment, autophagic processes, ER stress, and non-coding RNA regulation. Lastly, emerging therapeutic strategies that inhibit ferroptosis to mitigate MIRI are reviewed, providing new insights into potential clinical applications.

    Keywords: ferroptosis, Myocardial ischemia-reperfusion injury, Reactive Oxygen Species, iron metabolism, Lipid Peroxidation, therapeutic strategies

    Received: 19 Aug 2024; Accepted: 12 Sep 2024.

    Copyright: © 2024 Jin, Zhang, Zhang, Yang, Wang, Xu, Zhu, Jiang, Mi and Sun. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence:
    Binwei Jin, Department of Cardiology, Zhejiang Taizhou Hospital, Taizhou, 317000, China
    Zhiming Zhang, Department of Cardiology, Zhejiang Taizhou Hospital, Taizhou, 317000, China
    Yang Zhang, Department of Cardiology, Zhejiang Taizhou Hospital, Taizhou, 317000, China
    Minjun Yang, Department of Cardiology, Zhejiang Taizhou Hospital, Taizhou, 317000, China
    Cheng Wang, Department of Cardiology, Zhejiang Taizhou Hospital, Taizhou, 317000, China
    Jiayi Xu, Department of Cardiology, Zhejiang Taizhou Hospital, Taizhou, 317000, China
    Yu Zhu, Department of Cardiology, Zhejiang Taizhou Hospital, Taizhou, 317000, China
    Jianjun Jiang, Department of Cardiology, Taizhou Hospital, Wenzhou Medical University, Linhai, 325035, Zhejiang Province, China
    Yafei Mi, Department of Cardiology, Zhejiang Taizhou Hospital, Taizhou, 317000, China
    Zhenzhu Sun, Department of Cardiology, Zhejiang Taizhou Hospital, Taizhou, 317000, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.