Deciphering ferroptosis in critical care: mechanisms, consequences, and therapeutic opportunities

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 t...

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Main Authors: Ruimin Tan, Chen Ge, Yating Yan, He Guo, Xumin Han, Qiong Zhu, Quansheng Du
Format: Article
Language:English
Published: Frontiers Media S.A. 2024-12-01
Series:Frontiers in Immunology
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Online Access:https://www.frontiersin.org/articles/10.3389/fimmu.2024.1511015/full
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author Ruimin Tan
Ruimin Tan
Chen Ge
Yating Yan
Yating Yan
He Guo
He Guo
Xumin Han
Xumin Han
Qiong Zhu
Quansheng Du
author_facet Ruimin Tan
Ruimin Tan
Chen Ge
Yating Yan
Yating Yan
He Guo
He Guo
Xumin Han
Xumin Han
Qiong Zhu
Quansheng Du
author_sort Ruimin Tan
collection DOAJ
description 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.
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spelling doaj-art-06d198f8df7145aab74d258aa0a7208a2025-08-20T02:49:05ZengFrontiers Media S.A.Frontiers in Immunology1664-32242024-12-011510.3389/fimmu.2024.15110151511015Deciphering ferroptosis in critical care: mechanisms, consequences, and therapeutic opportunitiesRuimin Tan0Ruimin Tan1Chen Ge2Yating Yan3Yating Yan4He Guo5He Guo6Xumin Han7Xumin Han8Qiong Zhu9Quansheng Du10School of Clinical Medical, North China University of Science and Technology, Tangshan, Hebei, ChinaCritical Care Department, Hebei General Hospital, Shijiazhuang, Hebei, ChinaCritical Care Department, Hebei General Hospital, Shijiazhuang, Hebei, ChinaSchool of Clinical Medical, North China University of Science and Technology, Tangshan, Hebei, ChinaCritical Care Department, Hebei General Hospital, Shijiazhuang, Hebei, ChinaCritical Care Department, Hebei General Hospital, Shijiazhuang, Hebei, ChinaSchool of Graduate, Hebei Medical University, Shijiazhuang, Hebei, ChinaCritical Care Department, Hebei General Hospital, Shijiazhuang, Hebei, ChinaSchool of Graduate, Hebei Medical University, Shijiazhuang, Hebei, ChinaDepartment of Orthopaedics, The People’s Hospital Of Shizhu, Chongqing, ChinaCritical Care Department, Hebei General Hospital, Shijiazhuang, Hebei, ChinaIschemia-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.https://www.frontiersin.org/articles/10.3389/fimmu.2024.1511015/fullferroptosiscritical illnessiron overloadlipid metabolismmitochondrial dysfunction
spellingShingle Ruimin Tan
Ruimin Tan
Chen Ge
Yating Yan
Yating Yan
He Guo
He Guo
Xumin Han
Xumin Han
Qiong Zhu
Quansheng Du
Deciphering ferroptosis in critical care: mechanisms, consequences, and therapeutic opportunities
Frontiers in Immunology
ferroptosis
critical illness
iron overload
lipid metabolism
mitochondrial dysfunction
title Deciphering ferroptosis in critical care: mechanisms, consequences, and therapeutic opportunities
title_full Deciphering ferroptosis in critical care: mechanisms, consequences, and therapeutic opportunities
title_fullStr Deciphering ferroptosis in critical care: mechanisms, consequences, and therapeutic opportunities
title_full_unstemmed Deciphering ferroptosis in critical care: mechanisms, consequences, and therapeutic opportunities
title_short Deciphering ferroptosis in critical care: mechanisms, consequences, and therapeutic opportunities
title_sort deciphering ferroptosis in critical care mechanisms consequences and therapeutic opportunities
topic ferroptosis
critical illness
iron overload
lipid metabolism
mitochondrial dysfunction
url https://www.frontiersin.org/articles/10.3389/fimmu.2024.1511015/full
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