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Mitochondrial dysfunction and quality control lie at the heart of subarachnoid hemorrhage
The dramatic increase in intracranial pressure after subarachnoid hemorrhage leads to a decrease in cerebral perfusion pressure and a reduction in cerebral blood flow. Mitochondria are directly affected by direct factors such as ischemia, hypoxia, excitotoxicity, and toxicity of free hemoglobin and...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Wolters Kluwer - Medknow
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10664111/ https://www.ncbi.nlm.nih.gov/pubmed/37843218 http://dx.doi.org/10.4103/1673-5374.381493 |
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author | Zhang, Jiatong Zhu, Qi Wang, Jie Peng, Zheng Zhuang, Zong Hang, Chunhua Li, Wei |
author_facet | Zhang, Jiatong Zhu, Qi Wang, Jie Peng, Zheng Zhuang, Zong Hang, Chunhua Li, Wei |
author_sort | Zhang, Jiatong |
collection | PubMed |
description | The dramatic increase in intracranial pressure after subarachnoid hemorrhage leads to a decrease in cerebral perfusion pressure and a reduction in cerebral blood flow. Mitochondria are directly affected by direct factors such as ischemia, hypoxia, excitotoxicity, and toxicity of free hemoglobin and its degradation products, which trigger mitochondrial dysfunction. Dysfunctional mitochondria release large amounts of reactive oxygen species, inflammatory mediators, and apoptotic proteins that activate apoptotic pathways, further damaging cells. In response to this array of damage, cells have adopted multiple mitochondrial quality control mechanisms through evolution, including mitochondrial protein quality control, mitochondrial dynamics, mitophagy, mitochondrial biogenesis, and intercellular mitochondrial transfer, to maintain mitochondrial homeostasis under pathological conditions. Specific interventions targeting mitochondrial quality control mechanisms have emerged as promising therapeutic strategies for subarachnoid hemorrhage. This review provides an overview of recent research advances in mitochondrial pathophysiological processes after subarachnoid hemorrhage, particularly mitochondrial quality control mechanisms. It also presents potential therapeutic strategies to target mitochondrial quality control in subarachnoid hemorrhage. |
format | Online Article Text |
id | pubmed-10664111 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Wolters Kluwer - Medknow |
record_format | MEDLINE/PubMed |
spelling | pubmed-106641112023-07-20 Mitochondrial dysfunction and quality control lie at the heart of subarachnoid hemorrhage Zhang, Jiatong Zhu, Qi Wang, Jie Peng, Zheng Zhuang, Zong Hang, Chunhua Li, Wei Neural Regen Res Review The dramatic increase in intracranial pressure after subarachnoid hemorrhage leads to a decrease in cerebral perfusion pressure and a reduction in cerebral blood flow. Mitochondria are directly affected by direct factors such as ischemia, hypoxia, excitotoxicity, and toxicity of free hemoglobin and its degradation products, which trigger mitochondrial dysfunction. Dysfunctional mitochondria release large amounts of reactive oxygen species, inflammatory mediators, and apoptotic proteins that activate apoptotic pathways, further damaging cells. In response to this array of damage, cells have adopted multiple mitochondrial quality control mechanisms through evolution, including mitochondrial protein quality control, mitochondrial dynamics, mitophagy, mitochondrial biogenesis, and intercellular mitochondrial transfer, to maintain mitochondrial homeostasis under pathological conditions. Specific interventions targeting mitochondrial quality control mechanisms have emerged as promising therapeutic strategies for subarachnoid hemorrhage. This review provides an overview of recent research advances in mitochondrial pathophysiological processes after subarachnoid hemorrhage, particularly mitochondrial quality control mechanisms. It also presents potential therapeutic strategies to target mitochondrial quality control in subarachnoid hemorrhage. Wolters Kluwer - Medknow 2023-07-20 /pmc/articles/PMC10664111/ /pubmed/37843218 http://dx.doi.org/10.4103/1673-5374.381493 Text en Copyright: © Neural Regeneration Research https://creativecommons.org/licenses/by-nc-sa/4.0/This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms. |
spellingShingle | Review Zhang, Jiatong Zhu, Qi Wang, Jie Peng, Zheng Zhuang, Zong Hang, Chunhua Li, Wei Mitochondrial dysfunction and quality control lie at the heart of subarachnoid hemorrhage |
title | Mitochondrial dysfunction and quality control lie at the heart of subarachnoid hemorrhage |
title_full | Mitochondrial dysfunction and quality control lie at the heart of subarachnoid hemorrhage |
title_fullStr | Mitochondrial dysfunction and quality control lie at the heart of subarachnoid hemorrhage |
title_full_unstemmed | Mitochondrial dysfunction and quality control lie at the heart of subarachnoid hemorrhage |
title_short | Mitochondrial dysfunction and quality control lie at the heart of subarachnoid hemorrhage |
title_sort | mitochondrial dysfunction and quality control lie at the heart of subarachnoid hemorrhage |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10664111/ https://www.ncbi.nlm.nih.gov/pubmed/37843218 http://dx.doi.org/10.4103/1673-5374.381493 |
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