The autophagy–lysosomal system in subarachnoid haemorrhage
The autophagy–lysosomal pathway is a self‐catabolic process by which dysfunctional or unnecessary intracellular components are degraded by lysosomal enzymes. Proper function of this pathway is critical for maintaining cell homeostasis and survival. Subarachnoid haemorrhage (SAH) is one of the most d...
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Veröffentlicht in: | Journal of cellular and molecular medicine 2016-09, Vol.20 (9), p.1770-1778 |
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creator | Wu, Haijian Niu, Huanjiang Wu, Cheng Li, Yong Wang, Kun Zhang, Jianmin Wang, Yirong Yang, Shuxu |
description | The autophagy–lysosomal pathway is a self‐catabolic process by which dysfunctional or unnecessary intracellular components are degraded by lysosomal enzymes. Proper function of this pathway is critical for maintaining cell homeostasis and survival. Subarachnoid haemorrhage (SAH) is one of the most devastating forms of stroke. Multiple pathogenic mechanisms, such as inflammation, apoptosis, and oxidative stress, are all responsible for brain injury and poor outcome after SAH. Most recently, accumulating evidence has demonstrated that the autophagy–lysosomal pathway plays a crucial role in the pathophysiological process after SAH. Appropriate activity of autophagy–lysosomal pathway acts as a pro‐survival mechanism in SAH, while excessive self‐digestion results in cell death after SAH. Consequently, in this review article, we will give an overview of the pathophysiological roles of autophagy–lysosomal pathway in the pathogenesis of SAH. And approaching the molecular mechanisms underlying this pathway in SAH pathology is anticipated, which may ultimately allow development of effective therapeutic strategies for SAH patients through regulating the autophagy–lysosomal machinery. |
doi_str_mv | 10.1111/jcmm.12855 |
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Proper function of this pathway is critical for maintaining cell homeostasis and survival. Subarachnoid haemorrhage (SAH) is one of the most devastating forms of stroke. Multiple pathogenic mechanisms, such as inflammation, apoptosis, and oxidative stress, are all responsible for brain injury and poor outcome after SAH. Most recently, accumulating evidence has demonstrated that the autophagy–lysosomal pathway plays a crucial role in the pathophysiological process after SAH. Appropriate activity of autophagy–lysosomal pathway acts as a pro‐survival mechanism in SAH, while excessive self‐digestion results in cell death after SAH. Consequently, in this review article, we will give an overview of the pathophysiological roles of autophagy–lysosomal pathway in the pathogenesis of SAH. And approaching the molecular mechanisms underlying this pathway in SAH pathology is anticipated, which may ultimately allow development of effective therapeutic strategies for SAH patients through regulating the autophagy–lysosomal machinery.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.12855</identifier><identifier>PMID: 27027405</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Aneurysms ; Animals ; Apoptosis ; Autophagy ; Brain Injuries - complications ; Brain Injuries - pathology ; Brain injury ; Cathepsins - metabolism ; Cell death ; Cell survival ; Endoplasmic reticulum ; Enzymes ; Homeostasis ; Humans ; Kinases ; Lysosomal enzymes ; lysosome ; Lysosomes - metabolism ; Models, Biological ; Molecular modelling ; neuroprotection ; Oxidative stress ; Pathogenesis ; Pathology ; Phagocytosis ; Phosphorylation ; Proteins ; Review ; Rodents ; Stroke ; subarachnoid haemorrhage ; Subarachnoid hemorrhage ; Subarachnoid Hemorrhage - complications ; Subarachnoid Hemorrhage - metabolism ; Subarachnoid Hemorrhage - pathology ; Subarachnoid Hemorrhage - therapy ; Survival ; Traumatic brain injury</subject><ispartof>Journal of cellular and molecular medicine, 2016-09, Vol.20 (9), p.1770-1778</ispartof><rights>2016 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.</rights><rights>2016. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4485-54e70783fdd27814eedf123eb925f793b5f88801bca5543d35ef03fe58132da23</citedby><cites>FETCH-LOGICAL-c4485-54e70783fdd27814eedf123eb925f793b5f88801bca5543d35ef03fe58132da23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4988275/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4988275/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,1411,11541,27901,27902,45550,45551,46027,46451,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27027405$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, Haijian</creatorcontrib><creatorcontrib>Niu, Huanjiang</creatorcontrib><creatorcontrib>Wu, Cheng</creatorcontrib><creatorcontrib>Li, Yong</creatorcontrib><creatorcontrib>Wang, Kun</creatorcontrib><creatorcontrib>Zhang, Jianmin</creatorcontrib><creatorcontrib>Wang, Yirong</creatorcontrib><creatorcontrib>Yang, Shuxu</creatorcontrib><title>The autophagy–lysosomal system in subarachnoid haemorrhage</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>The autophagy–lysosomal pathway is a self‐catabolic process by which dysfunctional or unnecessary intracellular components are degraded by lysosomal enzymes. Proper function of this pathway is critical for maintaining cell homeostasis and survival. Subarachnoid haemorrhage (SAH) is one of the most devastating forms of stroke. Multiple pathogenic mechanisms, such as inflammation, apoptosis, and oxidative stress, are all responsible for brain injury and poor outcome after SAH. Most recently, accumulating evidence has demonstrated that the autophagy–lysosomal pathway plays a crucial role in the pathophysiological process after SAH. Appropriate activity of autophagy–lysosomal pathway acts as a pro‐survival mechanism in SAH, while excessive self‐digestion results in cell death after SAH. Consequently, in this review article, we will give an overview of the pathophysiological roles of autophagy–lysosomal pathway in the pathogenesis of SAH. And approaching the molecular mechanisms underlying this pathway in SAH pathology is anticipated, which may ultimately allow development of effective therapeutic strategies for SAH patients through regulating the autophagy–lysosomal machinery.</description><subject>Aneurysms</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Autophagy</subject><subject>Brain Injuries - complications</subject><subject>Brain Injuries - pathology</subject><subject>Brain injury</subject><subject>Cathepsins - metabolism</subject><subject>Cell death</subject><subject>Cell survival</subject><subject>Endoplasmic reticulum</subject><subject>Enzymes</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Kinases</subject><subject>Lysosomal enzymes</subject><subject>lysosome</subject><subject>Lysosomes - metabolism</subject><subject>Models, Biological</subject><subject>Molecular modelling</subject><subject>neuroprotection</subject><subject>Oxidative stress</subject><subject>Pathogenesis</subject><subject>Pathology</subject><subject>Phagocytosis</subject><subject>Phosphorylation</subject><subject>Proteins</subject><subject>Review</subject><subject>Rodents</subject><subject>Stroke</subject><subject>subarachnoid haemorrhage</subject><subject>Subarachnoid hemorrhage</subject><subject>Subarachnoid Hemorrhage - complications</subject><subject>Subarachnoid Hemorrhage - metabolism</subject><subject>Subarachnoid Hemorrhage - pathology</subject><subject>Subarachnoid Hemorrhage - therapy</subject><subject>Survival</subject><subject>Traumatic brain injury</subject><issn>1582-1838</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kc1Kw0AQxxdRbK1efAAJeBGhdT-bDYggxU8qXup52SSTJiXJ1t1Gyc138A19Ere2FvXgXmZhfvyYmT9ChwQPiH9ns6SqBoRKIbZQlwhJ-zxifHv9J5LJDtpzboYxGxIW7aIODTENORZddD7JIdDNwsxzPW0_3t7L1hlnKl0GrnULqIKiDlwTa6uTvDZFGuQaKmOtx2Ef7WS6dHCwrj30dH01Gd32x483d6PLcT_hXIq-4BDiULIsTWkoCQdIM0IZxBEVWRixWGRSSkziRAvBWcoEZJhlICRhNNWU9dDFyjtv4grSBOqF1aWa26LStlVGF-p3py5yNTUvikdS0lB4wclaYM1zA26hqsIlUJa6BtM4RaQ_n2R0OPTo8R90Zhpb-_UUpX4bjEO6FJ6uqMQa5yxkm2EIVstQ1DIU9RWKh49-jr9Bv1PwAFkBr0UJ7T8qdT96eFhJPwGY2Jih</recordid><startdate>201609</startdate><enddate>201609</enddate><creator>Wu, Haijian</creator><creator>Niu, Huanjiang</creator><creator>Wu, Cheng</creator><creator>Li, Yong</creator><creator>Wang, Kun</creator><creator>Zhang, Jianmin</creator><creator>Wang, Yirong</creator><creator>Yang, Shuxu</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201609</creationdate><title>The autophagy–lysosomal system in subarachnoid haemorrhage</title><author>Wu, Haijian ; Niu, Huanjiang ; Wu, Cheng ; Li, Yong ; Wang, Kun ; Zhang, Jianmin ; Wang, Yirong ; Yang, Shuxu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4485-54e70783fdd27814eedf123eb925f793b5f88801bca5543d35ef03fe58132da23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Aneurysms</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Autophagy</topic><topic>Brain Injuries - complications</topic><topic>Brain Injuries - pathology</topic><topic>Brain injury</topic><topic>Cathepsins - metabolism</topic><topic>Cell death</topic><topic>Cell survival</topic><topic>Endoplasmic reticulum</topic><topic>Enzymes</topic><topic>Homeostasis</topic><topic>Humans</topic><topic>Kinases</topic><topic>Lysosomal enzymes</topic><topic>lysosome</topic><topic>Lysosomes - metabolism</topic><topic>Models, Biological</topic><topic>Molecular modelling</topic><topic>neuroprotection</topic><topic>Oxidative stress</topic><topic>Pathogenesis</topic><topic>Pathology</topic><topic>Phagocytosis</topic><topic>Phosphorylation</topic><topic>Proteins</topic><topic>Review</topic><topic>Rodents</topic><topic>Stroke</topic><topic>subarachnoid haemorrhage</topic><topic>Subarachnoid hemorrhage</topic><topic>Subarachnoid Hemorrhage - complications</topic><topic>Subarachnoid Hemorrhage - metabolism</topic><topic>Subarachnoid Hemorrhage - pathology</topic><topic>Subarachnoid Hemorrhage - therapy</topic><topic>Survival</topic><topic>Traumatic brain injury</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wu, Haijian</creatorcontrib><creatorcontrib>Niu, Huanjiang</creatorcontrib><creatorcontrib>Wu, Cheng</creatorcontrib><creatorcontrib>Li, Yong</creatorcontrib><creatorcontrib>Wang, Kun</creatorcontrib><creatorcontrib>Zhang, Jianmin</creatorcontrib><creatorcontrib>Wang, Yirong</creatorcontrib><creatorcontrib>Yang, Shuxu</creatorcontrib><collection>Wiley Online Library Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of cellular and molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, Haijian</au><au>Niu, Huanjiang</au><au>Wu, Cheng</au><au>Li, Yong</au><au>Wang, Kun</au><au>Zhang, Jianmin</au><au>Wang, Yirong</au><au>Yang, Shuxu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The autophagy–lysosomal system in subarachnoid haemorrhage</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2016-09</date><risdate>2016</risdate><volume>20</volume><issue>9</issue><spage>1770</spage><epage>1778</epage><pages>1770-1778</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><abstract>The autophagy–lysosomal pathway is a self‐catabolic process by which dysfunctional or unnecessary intracellular components are degraded by lysosomal enzymes. Proper function of this pathway is critical for maintaining cell homeostasis and survival. Subarachnoid haemorrhage (SAH) is one of the most devastating forms of stroke. Multiple pathogenic mechanisms, such as inflammation, apoptosis, and oxidative stress, are all responsible for brain injury and poor outcome after SAH. Most recently, accumulating evidence has demonstrated that the autophagy–lysosomal pathway plays a crucial role in the pathophysiological process after SAH. Appropriate activity of autophagy–lysosomal pathway acts as a pro‐survival mechanism in SAH, while excessive self‐digestion results in cell death after SAH. Consequently, in this review article, we will give an overview of the pathophysiological roles of autophagy–lysosomal pathway in the pathogenesis of SAH. And approaching the molecular mechanisms underlying this pathway in SAH pathology is anticipated, which may ultimately allow development of effective therapeutic strategies for SAH patients through regulating the autophagy–lysosomal machinery.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>27027405</pmid><doi>10.1111/jcmm.12855</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Aneurysms Animals Apoptosis Autophagy Brain Injuries - complications Brain Injuries - pathology Brain injury Cathepsins - metabolism Cell death Cell survival Endoplasmic reticulum Enzymes Homeostasis Humans Kinases Lysosomal enzymes lysosome Lysosomes - metabolism Models, Biological Molecular modelling neuroprotection Oxidative stress Pathogenesis Pathology Phagocytosis Phosphorylation Proteins Review Rodents Stroke subarachnoid haemorrhage Subarachnoid hemorrhage Subarachnoid Hemorrhage - complications Subarachnoid Hemorrhage - metabolism Subarachnoid Hemorrhage - pathology Subarachnoid Hemorrhage - therapy Survival Traumatic brain injury |
title | The autophagy–lysosomal system in subarachnoid haemorrhage |
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