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The Role of Autophagy in Subarachnoid Hemorrhage: An Update

BACKGROUND: Autophagy is an extensive self-degradation process for the disposition of cytosolic aggregated or misfolded proteins and defective organelles which executes the functions of pro-survival and pro-death to maintain cellular homeostasis. The pathway plays essential roles in several neurolog...

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Autores principales: Fang, Yuanjian, Chen, Sheng, Reis, Cesar, Zhang, Jianmin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Bentham Science Publishers 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6251055/
https://www.ncbi.nlm.nih.gov/pubmed/28382869
http://dx.doi.org/10.2174/1570159X15666170406142631
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author Fang, Yuanjian
Chen, Sheng
Reis, Cesar
Zhang, Jianmin
author_facet Fang, Yuanjian
Chen, Sheng
Reis, Cesar
Zhang, Jianmin
author_sort Fang, Yuanjian
collection PubMed
description BACKGROUND: Autophagy is an extensive self-degradation process for the disposition of cytosolic aggregated or misfolded proteins and defective organelles which executes the functions of pro-survival and pro-death to maintain cellular homeostasis. The pathway plays essential roles in several neurological disorders. Subarachnoid Hemorrhage (SAH) is a devastating subtype of hemorrhagic stroke with high risk of neurological deficit and high mortality. Early brain injury (EBI) plays a role in the poor clinical course and outcome after SAH. Recent studies have paid attention on the role of the autopha-gy pathway in the development of EBI after SAH. We aim to update the multifaceted roles of autophagy pathway in the pathogenesis of SAH, especially in the phase of EBI. METHODS: We reviewed early researches related to autophagy and SAH. The following three aspects of contents will be mainly discussed: the process of the autophagy pathway, the role of the autophagy in SAH and the interaction between organelle dysfunction and autophagy pathway after SAH. RESULTS: Accumulating evidence shows an increased autophagy reaction in response to early stages of SAH. However, oth-ers suggest inadequate or excessive autophagy activation can result in cell injury and death. In addition to autophagy, apopto-sis and necrosis can occur in neurons simultaneously after SAH, leading to mixed features of cell death morphologies. And it is also known that there is extensive crosstalk between autophagy and apoptosis pathway. Subcellular organelles of neural cells generally participate in the formation and functional parts of autophagy process. CONCLUSION: Autophagy plays an important role in the SAH-induced brain injury. A better understanding of the interrelationship among autophagy, apoptosis, and necrosis might provide us better therapeutic targets for the treatment of SAH
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spelling pubmed-62510552019-05-01 The Role of Autophagy in Subarachnoid Hemorrhage: An Update Fang, Yuanjian Chen, Sheng Reis, Cesar Zhang, Jianmin Curr Neuropharmacol Article BACKGROUND: Autophagy is an extensive self-degradation process for the disposition of cytosolic aggregated or misfolded proteins and defective organelles which executes the functions of pro-survival and pro-death to maintain cellular homeostasis. The pathway plays essential roles in several neurological disorders. Subarachnoid Hemorrhage (SAH) is a devastating subtype of hemorrhagic stroke with high risk of neurological deficit and high mortality. Early brain injury (EBI) plays a role in the poor clinical course and outcome after SAH. Recent studies have paid attention on the role of the autopha-gy pathway in the development of EBI after SAH. We aim to update the multifaceted roles of autophagy pathway in the pathogenesis of SAH, especially in the phase of EBI. METHODS: We reviewed early researches related to autophagy and SAH. The following three aspects of contents will be mainly discussed: the process of the autophagy pathway, the role of the autophagy in SAH and the interaction between organelle dysfunction and autophagy pathway after SAH. RESULTS: Accumulating evidence shows an increased autophagy reaction in response to early stages of SAH. However, oth-ers suggest inadequate or excessive autophagy activation can result in cell injury and death. In addition to autophagy, apopto-sis and necrosis can occur in neurons simultaneously after SAH, leading to mixed features of cell death morphologies. And it is also known that there is extensive crosstalk between autophagy and apoptosis pathway. Subcellular organelles of neural cells generally participate in the formation and functional parts of autophagy process. CONCLUSION: Autophagy plays an important role in the SAH-induced brain injury. A better understanding of the interrelationship among autophagy, apoptosis, and necrosis might provide us better therapeutic targets for the treatment of SAH Bentham Science Publishers 2018-11 2018-11 /pmc/articles/PMC6251055/ /pubmed/28382869 http://dx.doi.org/10.2174/1570159X15666170406142631 Text en © 2018 Bentham Science Publishers https://creativecommons.org/licenses/by-nc/4.0/legalcode This is an open access article licensed under the terms of the Creative Commons Attribution-Non-Commercial 4.0 International Public License (CC BY-NC 4.0) (https://creativecommons.org/licenses/by-nc/4.0/legalcode), which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.
spellingShingle Article
Fang, Yuanjian
Chen, Sheng
Reis, Cesar
Zhang, Jianmin
The Role of Autophagy in Subarachnoid Hemorrhage: An Update
title The Role of Autophagy in Subarachnoid Hemorrhage: An Update
title_full The Role of Autophagy in Subarachnoid Hemorrhage: An Update
title_fullStr The Role of Autophagy in Subarachnoid Hemorrhage: An Update
title_full_unstemmed The Role of Autophagy in Subarachnoid Hemorrhage: An Update
title_short The Role of Autophagy in Subarachnoid Hemorrhage: An Update
title_sort role of autophagy in subarachnoid hemorrhage: an update
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6251055/
https://www.ncbi.nlm.nih.gov/pubmed/28382869
http://dx.doi.org/10.2174/1570159X15666170406142631
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