The mitochondria as a potential therapeutic target in cerebral I/R injury
Ischemic stroke is a major cause of mortality and disability worldwide. Among patients with ischemic stroke, the primary treatment goal is to reduce acute cerebral ischemic injury and limit the infarct size in a timely manner by ensuring effective cerebral reperfusion through the administration of e...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2025-01-01
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| Series: | Frontiers in Neuroscience |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fnins.2024.1500647/full |
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| author | Susu Fang Susu Fang Wenzhou Huang Wenzhou Huang Xinhui Qu Xinhui Qu Wen Chai |
| author_facet | Susu Fang Susu Fang Wenzhou Huang Wenzhou Huang Xinhui Qu Xinhui Qu Wen Chai |
| author_sort | Susu Fang |
| collection | DOAJ |
| description | Ischemic stroke is a major cause of mortality and disability worldwide. Among patients with ischemic stroke, the primary treatment goal is to reduce acute cerebral ischemic injury and limit the infarct size in a timely manner by ensuring effective cerebral reperfusion through the administration of either intravenous thrombolysis or endovascular therapy. However, reperfusion can induce neuronal death, known as cerebral reperfusion injury, for which effective therapies are lacking. Accumulating data supports a paradigm whereby cerebral ischemia/reperfusion (I/R) injury is coupled with impaired mitochondrial function, contributing to the pathogenesis of ischemic stroke. Herein, we review recent evidence demonstrating a heterogeneous mitochondrial response following cerebral I/R injury, placing a specific focus on mitochondrial protein modifications, reactive oxygen species, calcium (Ca2+), inflammation, and quality control under experimental conditions using animal models. |
| format | Article |
| id | doaj-art-ed7a1cc91b6241b19c71b93ace79381e |
| institution | Kabale University |
| issn | 1662-453X |
| language | English |
| publishDate | 2025-01-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Neuroscience |
| spelling | doaj-art-ed7a1cc91b6241b19c71b93ace79381e2025-01-07T06:40:25ZengFrontiers Media S.A.Frontiers in Neuroscience1662-453X2025-01-011810.3389/fnins.2024.15006471500647The mitochondria as a potential therapeutic target in cerebral I/R injurySusu Fang0Susu Fang1Wenzhou Huang2Wenzhou Huang3Xinhui Qu4Xinhui Qu5Wen Chai6The Second Department of Neurology, Jiangxi Provincial People’s Hospital and The First Affiliated Hospital of Nanchang Medical College, Nanchang, Jiangxi, ChinaInstitute of Geriatrics, Jiangxi Provincial People’s Hospital, The First Affiliated Hospital of Nanchang Medical College, Nanchang, Jiangxi, ChinaDepartment of Orthopedics, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, ChinaJiangxi Provincial Key Laboratory of Spine and Spinal Cord Disease, Nanchang, Jiangxi, ChinaThe Second Department of Neurology, Jiangxi Provincial People’s Hospital and The First Affiliated Hospital of Nanchang Medical College, Nanchang, Jiangxi, ChinaInstitute of Geriatrics, Jiangxi Provincial People’s Hospital, The First Affiliated Hospital of Nanchang Medical College, Nanchang, Jiangxi, ChinaDepartment of Neurology, Jiangxi Provincial People’s Hospital, The First Affiliated Hospital of Nanchang Medical College, Nanchang, Jiangxi, ChinaIschemic stroke is a major cause of mortality and disability worldwide. Among patients with ischemic stroke, the primary treatment goal is to reduce acute cerebral ischemic injury and limit the infarct size in a timely manner by ensuring effective cerebral reperfusion through the administration of either intravenous thrombolysis or endovascular therapy. However, reperfusion can induce neuronal death, known as cerebral reperfusion injury, for which effective therapies are lacking. Accumulating data supports a paradigm whereby cerebral ischemia/reperfusion (I/R) injury is coupled with impaired mitochondrial function, contributing to the pathogenesis of ischemic stroke. Herein, we review recent evidence demonstrating a heterogeneous mitochondrial response following cerebral I/R injury, placing a specific focus on mitochondrial protein modifications, reactive oxygen species, calcium (Ca2+), inflammation, and quality control under experimental conditions using animal models.https://www.frontiersin.org/articles/10.3389/fnins.2024.1500647/fullcerebral ischemia/reperfusion injury (CIRI)mitochondrionacetylationCa2+ROSinflammation |
| spellingShingle | Susu Fang Susu Fang Wenzhou Huang Wenzhou Huang Xinhui Qu Xinhui Qu Wen Chai The mitochondria as a potential therapeutic target in cerebral I/R injury Frontiers in Neuroscience cerebral ischemia/reperfusion injury (CIRI) mitochondrion acetylation Ca2+ ROS inflammation |
| title | The mitochondria as a potential therapeutic target in cerebral I/R injury |
| title_full | The mitochondria as a potential therapeutic target in cerebral I/R injury |
| title_fullStr | The mitochondria as a potential therapeutic target in cerebral I/R injury |
| title_full_unstemmed | The mitochondria as a potential therapeutic target in cerebral I/R injury |
| title_short | The mitochondria as a potential therapeutic target in cerebral I/R injury |
| title_sort | mitochondria as a potential therapeutic target in cerebral i r injury |
| topic | cerebral ischemia/reperfusion injury (CIRI) mitochondrion acetylation Ca2+ ROS inflammation |
| url | https://www.frontiersin.org/articles/10.3389/fnins.2024.1500647/full |
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