Mitochondrial stress: a key role of neuroinflammation in stroke
Abstract Stroke is a clinical syndrome characterized by an acute, focal neurological deficit, primarily caused by the occlusion or rupture of cerebral blood vessels. In stroke, neuroinflammation emerges as a pivotal event contributing to neuronal cell death. The occurrence and progression of neuroin...
| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
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BMC
2024-02-01
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| Series: | Journal of Neuroinflammation |
| Subjects: | |
| Online Access: | https://doi.org/10.1186/s12974-024-03033-7 |
| _version_ | 1797273732776984576 |
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| author | Ling Gao Li Peng Jian Wang John H. Zhang Ying Xia |
| author_facet | Ling Gao Li Peng Jian Wang John H. Zhang Ying Xia |
| author_sort | Ling Gao |
| collection | DOAJ |
| description | Abstract Stroke is a clinical syndrome characterized by an acute, focal neurological deficit, primarily caused by the occlusion or rupture of cerebral blood vessels. In stroke, neuroinflammation emerges as a pivotal event contributing to neuronal cell death. The occurrence and progression of neuroinflammation entail intricate processes, prominently featuring mitochondrial dysfunction and adaptive responses. Mitochondria, a double membrane-bound organelle are recognized as the “energy workshop” of the body. Brain is particularly vulnerable to mitochondrial disturbances due to its high energy demands from mitochondria-related energy production. The interplay between mitochondria and neuroinflammation plays a significant role in the pathogenesis of stroke. The biological and pathological consequences resulting from mitochondrial stress have substantial implications for cerebral function. Mitochondrial stress serves as an adaptive mechanism aimed at mitigating the stress induced by the import of misfolded proteins, which occurs in response to stroke. This adaptive response involves a reduction in misfolded protein accumulation and overall protein synthesis. The influence of mitochondrial stress on the pathological state of stroke is underscored by its capacity to interact with neuroinflammation. The impact of mitochondrial stress on neuroinflammation varies according to its severity. Moderate mitochondrial stress can bolster cellular adaptive defenses, enabling cells to better withstand detrimental stressors. In contrast, sustained and excessive mitochondrial stress detrimentally affects cellular and tissue integrity. The relationship between neuroinflammation and mitochondrial stress depends on the degree of mitochondrial stress present. Understanding its role in stroke pathogenesis is instrumental in excavating the novel treatment of stroke. This review aims to provide the evaluation of the cross-talk between mitochondrial stress and neuroinflammation within the context of stroke. We aim to reveal how mitochondrial stress affects neuroinflammation environment in stroke. |
| first_indexed | 2024-03-07T14:48:30Z |
| format | Article |
| id | doaj.art-4627602516364a5fb19ea28ab9338b83 |
| institution | Directory Open Access Journal |
| issn | 1742-2094 |
| language | English |
| last_indexed | 2024-03-07T14:48:30Z |
| publishDate | 2024-02-01 |
| publisher | BMC |
| record_format | Article |
| series | Journal of Neuroinflammation |
| spelling | doaj.art-4627602516364a5fb19ea28ab9338b832024-03-05T19:48:56ZengBMCJournal of Neuroinflammation1742-20942024-02-0121111510.1186/s12974-024-03033-7Mitochondrial stress: a key role of neuroinflammation in strokeLing Gao0Li Peng1Jian Wang2John H. Zhang3Ying Xia4Department of Neurosurgery, Xiangya School of Medicine, Affiliated Haikou Hospital, Central South UniversityDepartment of Ophthalmology, Xiangya School of Medicine, Affiliated Haikou Hospital, Central South UniversityDepartment of Neurosurgery, Xiangya School of Medicine, Affiliated Haikou Hospital, Central South UniversityDepartment of Physiology and Pharmacology, School of Medicine, Loma Linda UniversityDepartment of Neurosurgery, Xiangya School of Medicine, Affiliated Haikou Hospital, Central South UniversityAbstract Stroke is a clinical syndrome characterized by an acute, focal neurological deficit, primarily caused by the occlusion or rupture of cerebral blood vessels. In stroke, neuroinflammation emerges as a pivotal event contributing to neuronal cell death. The occurrence and progression of neuroinflammation entail intricate processes, prominently featuring mitochondrial dysfunction and adaptive responses. Mitochondria, a double membrane-bound organelle are recognized as the “energy workshop” of the body. Brain is particularly vulnerable to mitochondrial disturbances due to its high energy demands from mitochondria-related energy production. The interplay between mitochondria and neuroinflammation plays a significant role in the pathogenesis of stroke. The biological and pathological consequences resulting from mitochondrial stress have substantial implications for cerebral function. Mitochondrial stress serves as an adaptive mechanism aimed at mitigating the stress induced by the import of misfolded proteins, which occurs in response to stroke. This adaptive response involves a reduction in misfolded protein accumulation and overall protein synthesis. The influence of mitochondrial stress on the pathological state of stroke is underscored by its capacity to interact with neuroinflammation. The impact of mitochondrial stress on neuroinflammation varies according to its severity. Moderate mitochondrial stress can bolster cellular adaptive defenses, enabling cells to better withstand detrimental stressors. In contrast, sustained and excessive mitochondrial stress detrimentally affects cellular and tissue integrity. The relationship between neuroinflammation and mitochondrial stress depends on the degree of mitochondrial stress present. Understanding its role in stroke pathogenesis is instrumental in excavating the novel treatment of stroke. This review aims to provide the evaluation of the cross-talk between mitochondrial stress and neuroinflammation within the context of stroke. We aim to reveal how mitochondrial stress affects neuroinflammation environment in stroke.https://doi.org/10.1186/s12974-024-03033-7Mitochondrial stressMitophagyNeuroinflammationStroke |
| spellingShingle | Ling Gao Li Peng Jian Wang John H. Zhang Ying Xia Mitochondrial stress: a key role of neuroinflammation in stroke Journal of Neuroinflammation Mitochondrial stress Mitophagy Neuroinflammation Stroke |
| title | Mitochondrial stress: a key role of neuroinflammation in stroke |
| title_full | Mitochondrial stress: a key role of neuroinflammation in stroke |
| title_fullStr | Mitochondrial stress: a key role of neuroinflammation in stroke |
| title_full_unstemmed | Mitochondrial stress: a key role of neuroinflammation in stroke |
| title_short | Mitochondrial stress: a key role of neuroinflammation in stroke |
| title_sort | mitochondrial stress a key role of neuroinflammation in stroke |
| topic | Mitochondrial stress Mitophagy Neuroinflammation Stroke |
| url | https://doi.org/10.1186/s12974-024-03033-7 |
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