Mechanisms Associated with Mitophagy and Ferroptosis in Cerebral Ischemia-reperfusion Injury

Ischemic stroke (IS) constitutes a major threat to human health. Vascular recanalization by intravenous thrombolysis and mechanical thrombolysis remain the most significant and effective methods for relief of ischemia. Key elements of these treatments include achieving blood-vessel recanalization, r...

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Main Authors: Yugang Ma, Xuebin Wang, Yahui Li, Jing Zhao, Xue Zhou, Xingchen Wang
Format: Article
Language:English
Published: IMR Press 2025-03-01
Series:Journal of Integrative Neuroscience
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Online Access:https://www.imrpress.com/journal/JIN/24/3/10.31083/JIN26458
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author Yugang Ma
Xuebin Wang
Yahui Li
Jing Zhao
Xue Zhou
Xingchen Wang
author_facet Yugang Ma
Xuebin Wang
Yahui Li
Jing Zhao
Xue Zhou
Xingchen Wang
author_sort Yugang Ma
collection DOAJ
description Ischemic stroke (IS) constitutes a major threat to human health. Vascular recanalization by intravenous thrombolysis and mechanical thrombolysis remain the most significant and effective methods for relief of ischemia. Key elements of these treatments include achieving blood-vessel recanalization, restoring brain-tissue reperfusion, and preserving the ischemic penumbra. However, in achieving the therapeutic goals of vascular recanalization, secondary damage to brain tissue from cerebral ischemia-reperfusion injury (CIRI) must also be addressed. Despite advancements in understanding the pathological processes associated with CIRI, effective interventions to prevent its onset and progression are still lacking. Recent research has indicated that mitophagy and ferroptosis are critical mechanisms in the development of CIRI, and significantly contribute to the onset and progression of IS and CIRI because of common targets and co-occurrence mechanisms. Therefore, exploring and summarizing the potential connections between mitophagy and ferroptosis during CIRI is crucial. In the present review, we mainly focused on the mechanisms of mitochondrial autophagy and ferroptosis, and their interaction, in the development of CIRI. We believe that the data show a strong relationship between mitochondrial autophagy and ferroptosis with interactive regulation. This information may underpin new potential approaches for the prevention and treatment of IS and subsequent CIRI.
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institution Kabale University
issn 0219-6352
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publishDate 2025-03-01
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series Journal of Integrative Neuroscience
spelling doaj-art-e2559f226d634655880576326dae4e602025-08-20T03:42:23ZengIMR PressJournal of Integrative Neuroscience0219-63522025-03-012432645810.31083/JIN26458S0219-6352(24)00876-3Mechanisms Associated with Mitophagy and Ferroptosis in Cerebral Ischemia-reperfusion InjuryYugang Ma0Xuebin Wang1Yahui Li2Jing Zhao3Xue Zhou4Xingchen Wang5First Clinical Medical College, Shandong University of Traditional Chinese Medicine, 250014 Jinan, Shandong, ChinaPostdoctoral Research Station, Shandong University of Traditional Chinese Medicine, 250014 Jinan, Shandong, ChinaFirst Clinical Medical College, Shandong University of Traditional Chinese Medicine, 250014 Jinan, Shandong, ChinaFirst Clinical Medical College, Shandong University of Traditional Chinese Medicine, 250014 Jinan, Shandong, ChinaPostdoctoral Research Station, Shandong University of Traditional Chinese Medicine, 250014 Jinan, Shandong, ChinaDepartment of Neurology, The Second Affiliated Hospital of Shandong University of Traditional Chinese Medicine, 250001 Jinan, Shandong, ChinaIschemic stroke (IS) constitutes a major threat to human health. Vascular recanalization by intravenous thrombolysis and mechanical thrombolysis remain the most significant and effective methods for relief of ischemia. Key elements of these treatments include achieving blood-vessel recanalization, restoring brain-tissue reperfusion, and preserving the ischemic penumbra. However, in achieving the therapeutic goals of vascular recanalization, secondary damage to brain tissue from cerebral ischemia-reperfusion injury (CIRI) must also be addressed. Despite advancements in understanding the pathological processes associated with CIRI, effective interventions to prevent its onset and progression are still lacking. Recent research has indicated that mitophagy and ferroptosis are critical mechanisms in the development of CIRI, and significantly contribute to the onset and progression of IS and CIRI because of common targets and co-occurrence mechanisms. Therefore, exploring and summarizing the potential connections between mitophagy and ferroptosis during CIRI is crucial. In the present review, we mainly focused on the mechanisms of mitochondrial autophagy and ferroptosis, and their interaction, in the development of CIRI. We believe that the data show a strong relationship between mitochondrial autophagy and ferroptosis with interactive regulation. This information may underpin new potential approaches for the prevention and treatment of IS and subsequent CIRI.https://www.imrpress.com/journal/JIN/24/3/10.31083/JIN26458cerebral ischemia-reperfusion injurymitophagyferroptosisischemic strokemechanism research
spellingShingle Yugang Ma
Xuebin Wang
Yahui Li
Jing Zhao
Xue Zhou
Xingchen Wang
Mechanisms Associated with Mitophagy and Ferroptosis in Cerebral Ischemia-reperfusion Injury
Journal of Integrative Neuroscience
cerebral ischemia-reperfusion injury
mitophagy
ferroptosis
ischemic stroke
mechanism research
title Mechanisms Associated with Mitophagy and Ferroptosis in Cerebral Ischemia-reperfusion Injury
title_full Mechanisms Associated with Mitophagy and Ferroptosis in Cerebral Ischemia-reperfusion Injury
title_fullStr Mechanisms Associated with Mitophagy and Ferroptosis in Cerebral Ischemia-reperfusion Injury
title_full_unstemmed Mechanisms Associated with Mitophagy and Ferroptosis in Cerebral Ischemia-reperfusion Injury
title_short Mechanisms Associated with Mitophagy and Ferroptosis in Cerebral Ischemia-reperfusion Injury
title_sort mechanisms associated with mitophagy and ferroptosis in cerebral ischemia reperfusion injury
topic cerebral ischemia-reperfusion injury
mitophagy
ferroptosis
ischemic stroke
mechanism research
url https://www.imrpress.com/journal/JIN/24/3/10.31083/JIN26458
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AT yahuili mechanismsassociatedwithmitophagyandferroptosisincerebralischemiareperfusioninjury
AT jingzhao mechanismsassociatedwithmitophagyandferroptosisincerebralischemiareperfusioninjury
AT xuezhou mechanismsassociatedwithmitophagyandferroptosisincerebralischemiareperfusioninjury
AT xingchenwang mechanismsassociatedwithmitophagyandferroptosisincerebralischemiareperfusioninjury