Crosstalk between autophagy and ferroptosis mediate injury in ischemic stroke by generating reactive oxygen species
Stroke represents a significant threat to global human health, characterized by high rates of morbidity, disability, and mortality. Predominantly, strokes are ischemic in nature. Ischemic stroke (IS) is influenced by various cell death pathways, notably autophagy and ferroptosis. Recent studies have...
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| Format: | Article |
| Language: | English |
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Elsevier
2024-04-01
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| Series: | Heliyon |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S2405844024049909 |
| _version_ | 1797219357332340736 |
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| author | Xing-Yu Zhang Ping-Ping Han Yi-Ning Zhao Xin-Ya Shen Xia Bi |
| author_facet | Xing-Yu Zhang Ping-Ping Han Yi-Ning Zhao Xin-Ya Shen Xia Bi |
| author_sort | Xing-Yu Zhang |
| collection | DOAJ |
| description | Stroke represents a significant threat to global human health, characterized by high rates of morbidity, disability, and mortality. Predominantly, strokes are ischemic in nature. Ischemic stroke (IS) is influenced by various cell death pathways, notably autophagy and ferroptosis. Recent studies have increasingly highlighted the interplay between autophagy and ferroptosis, a process likely driven by the accumulation of reactive oxygen species (ROS). Post-IS, either the inhibition of autophagy or its excessive activation can escalate ROS levels. Concurrently, the interaction between ROS and lipids during ferroptosis further augments ROS accumulation. Elevated ROS levels can provoke endoplasmic reticulum stress-induced autophagy and, in conjunction with free iron (Fe2+), can trigger ferroptosis. Moreover, ROS contribute to protein and lipid oxidation, endothelial dysfunction, and an inflammatory response, all of which mediate secondary brain injury following IS. This review succinctly explores the mechanisms of ROS-mediated crosstalk between autophagy and ferroptosis and the detrimental impact of increased ROS on IS. It also offers novel perspectives for IS treatment strategies. |
| first_indexed | 2024-04-24T12:32:22Z |
| format | Article |
| id | doaj.art-e10587c086884cebae85224512ec6a78 |
| institution | Directory Open Access Journal |
| issn | 2405-8440 |
| language | English |
| last_indexed | 2024-04-24T12:32:22Z |
| publishDate | 2024-04-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Heliyon |
| spelling | doaj.art-e10587c086884cebae85224512ec6a782024-04-08T04:08:33ZengElsevierHeliyon2405-84402024-04-01107e28959Crosstalk between autophagy and ferroptosis mediate injury in ischemic stroke by generating reactive oxygen speciesXing-Yu Zhang0Ping-Ping Han1Yi-Ning Zhao2Xin-Ya Shen3Xia Bi4Department of Rehabilitation Medicine, Shanghai University of Medicine and Health Sciences Affiliated Zhoupu Hospital, Shanghai, China; Graduate School of Shanghai University of Traditional Chinese Medicine, Shanghai, ChinaDepartment of Rehabilitation Medicine, Shanghai University of Medicine and Health Sciences Affiliated Zhoupu Hospital, Shanghai, China; Department of Sport Rehabilitation, Shanghai University of Sport, Shanghai, ChinaDepartment of Rehabilitation Medicine, Shanghai University of Medicine and Health Sciences Affiliated Zhoupu Hospital, Shanghai, China; Department of Sport Rehabilitation, Shanghai University of Sport, Shanghai, ChinaDepartment of Rehabilitation Medicine, Shanghai University of Medicine and Health Sciences Affiliated Zhoupu Hospital, Shanghai, ChinaDepartment of Rehabilitation Medicine, Shanghai University of Medicine and Health Sciences Affiliated Zhoupu Hospital, Shanghai, China; Corresponding author.Stroke represents a significant threat to global human health, characterized by high rates of morbidity, disability, and mortality. Predominantly, strokes are ischemic in nature. Ischemic stroke (IS) is influenced by various cell death pathways, notably autophagy and ferroptosis. Recent studies have increasingly highlighted the interplay between autophagy and ferroptosis, a process likely driven by the accumulation of reactive oxygen species (ROS). Post-IS, either the inhibition of autophagy or its excessive activation can escalate ROS levels. Concurrently, the interaction between ROS and lipids during ferroptosis further augments ROS accumulation. Elevated ROS levels can provoke endoplasmic reticulum stress-induced autophagy and, in conjunction with free iron (Fe2+), can trigger ferroptosis. Moreover, ROS contribute to protein and lipid oxidation, endothelial dysfunction, and an inflammatory response, all of which mediate secondary brain injury following IS. This review succinctly explores the mechanisms of ROS-mediated crosstalk between autophagy and ferroptosis and the detrimental impact of increased ROS on IS. It also offers novel perspectives for IS treatment strategies.http://www.sciencedirect.com/science/article/pii/S2405844024049909AutophagyFerroptosisROSOxidative damageNeurological injuryIschemic stroke |
| spellingShingle | Xing-Yu Zhang Ping-Ping Han Yi-Ning Zhao Xin-Ya Shen Xia Bi Crosstalk between autophagy and ferroptosis mediate injury in ischemic stroke by generating reactive oxygen species Heliyon Autophagy Ferroptosis ROS Oxidative damage Neurological injury Ischemic stroke |
| title | Crosstalk between autophagy and ferroptosis mediate injury in ischemic stroke by generating reactive oxygen species |
| title_full | Crosstalk between autophagy and ferroptosis mediate injury in ischemic stroke by generating reactive oxygen species |
| title_fullStr | Crosstalk between autophagy and ferroptosis mediate injury in ischemic stroke by generating reactive oxygen species |
| title_full_unstemmed | Crosstalk between autophagy and ferroptosis mediate injury in ischemic stroke by generating reactive oxygen species |
| title_short | Crosstalk between autophagy and ferroptosis mediate injury in ischemic stroke by generating reactive oxygen species |
| title_sort | crosstalk between autophagy and ferroptosis mediate injury in ischemic stroke by generating reactive oxygen species |
| topic | Autophagy Ferroptosis ROS Oxidative damage Neurological injury Ischemic stroke |
| url | http://www.sciencedirect.com/science/article/pii/S2405844024049909 |
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