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REVIEW article

Front. Immunol.
Sec. Inflammation
Volume 15 - 2024 | doi: 10.3389/fimmu.2024.1511015
This article is part of the Research Topic Crosstalk in Ferroptosis, Immunity & Inflammation View all 13 articles

Deciphering Ferroptosis in Critical Care: Mechanisms, Consequences, and Therapeutic Opportunities

Provisionally accepted
Ruimin Tan Ruimin Tan 1Chen Ge Chen Ge 2*Yating Yan Yating Yan 1*He Guo He Guo 3Xumin Han Xumin Han 3*Qiong Zhu Qiong Zhu 4*Quansheng Du Quansheng Du 2*
  • 1 School of Clinical Medical, North China University of Science and Technology, Tangshan Hebei 063210, China, Tangshan, China
  • 2 Critical care department, Hebei General Hospital, Shijiazhuang Hebei 050051, China, Shijiazhuang, Hebei Province, China
  • 3 School of Graduate, Hebei Medical University, Shijiazhuang Hebei 050017, China, Shijiazhuang, Hebei Province, China
  • 4 Department of Orthopaedics, The People’s Hospital of Shizhu, Chongqing 409100, China, Chongqing, China

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

    Ischemia-reperfusion injuries (IRI) across various organs and tissues, along with sepsis, significantly contribute to the progression of critical illnesses. These conditions disrupt the balance of inflammatory mediators and signaling pathways, resulting in impaired physiological functions in human tissues and organs. Ferroptosis, a distinct form of programmed cell death, plays a pivotal role in regulating tissue damage and modulating inflammatory responses, thereby influencing the onset and progression of severe illnesses. Recent studies highlight that pharmacological agents targeting ferroptosis-related proteins can effectively mitigate oxidative stress caused by IRI in multiple organs, alleviating associated symptoms. This manuscript delves into the mechanisms and signaling pathways underlying ferroptosis, its role in critical illnesses, and its therapeutic potential in mitigating disease progression. We aim to offer a novel perspective for advancing clinical treatments for critical illnesses.

    Keywords: ferroptosis, Critical Illness, Iron Overload, Lipid Metabolism, Mitochondrial dysfunction

    Received: 14 Oct 2024; Accepted: 03 Dec 2024.

    Copyright: © 2024 Tan, Ge, Yan, Guo, Han, Zhu and Du. 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:
    Chen Ge, Critical care department, Hebei General Hospital, Shijiazhuang Hebei 050051, China, Shijiazhuang, Hebei Province, China
    Yating Yan, School of Clinical Medical, North China University of Science and Technology, Tangshan Hebei 063210, China, Tangshan, China
    Xumin Han, School of Graduate, Hebei Medical University, Shijiazhuang Hebei 050017, China, Shijiazhuang, Hebei Province, China
    Qiong Zhu, Department of Orthopaedics, The People’s Hospital of Shizhu, Chongqing 409100, China, Chongqing, China
    Quansheng Du, Critical care department, Hebei General Hospital, Shijiazhuang Hebei 050051, China, Shijiazhuang, Hebei Province, 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.