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Protective Role of mTOR in Liver Ischemia/Reperfusion Injury: Involvement of Inflammation and Autophagy

Liver ischemia/reperfusion (IR) injury is a common phenomenon after liver resection and transplantation, which often results in liver graft dysfunction such as delayed graft function and primary nonfunction. The mammalian target of rapamycin (mTOR) is an evolutionarily highly conserved serine/threon...

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Detalles Bibliográficos
Autores principales: Zhang, Tao, Guo, Jianrong, Gu, Jian, Chen, Ke, Li, Huili, Wang, Jiliang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6885218/
https://www.ncbi.nlm.nih.gov/pubmed/31827701
http://dx.doi.org/10.1155/2019/7861290
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author Zhang, Tao
Guo, Jianrong
Gu, Jian
Chen, Ke
Li, Huili
Wang, Jiliang
author_facet Zhang, Tao
Guo, Jianrong
Gu, Jian
Chen, Ke
Li, Huili
Wang, Jiliang
author_sort Zhang, Tao
collection PubMed
description Liver ischemia/reperfusion (IR) injury is a common phenomenon after liver resection and transplantation, which often results in liver graft dysfunction such as delayed graft function and primary nonfunction. The mammalian target of rapamycin (mTOR) is an evolutionarily highly conserved serine/threonine protein kinase, which coordinates cell growth and metabolism through sensing environmental inputs under physiological or pathological conditions, involved in the pathophysiological process of IR injury. In this review, we mainly present current evidence of the beneficial role of mTOR in modulating inflammation and autophagy under liver IR to provide some evidence for the potential therapies for liver IR injury.
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spelling pubmed-68852182019-12-11 Protective Role of mTOR in Liver Ischemia/Reperfusion Injury: Involvement of Inflammation and Autophagy Zhang, Tao Guo, Jianrong Gu, Jian Chen, Ke Li, Huili Wang, Jiliang Oxid Med Cell Longev Review Article Liver ischemia/reperfusion (IR) injury is a common phenomenon after liver resection and transplantation, which often results in liver graft dysfunction such as delayed graft function and primary nonfunction. The mammalian target of rapamycin (mTOR) is an evolutionarily highly conserved serine/threonine protein kinase, which coordinates cell growth and metabolism through sensing environmental inputs under physiological or pathological conditions, involved in the pathophysiological process of IR injury. In this review, we mainly present current evidence of the beneficial role of mTOR in modulating inflammation and autophagy under liver IR to provide some evidence for the potential therapies for liver IR injury. Hindawi 2019-11-13 /pmc/articles/PMC6885218/ /pubmed/31827701 http://dx.doi.org/10.1155/2019/7861290 Text en Copyright © 2019 Tao Zhang et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Zhang, Tao
Guo, Jianrong
Gu, Jian
Chen, Ke
Li, Huili
Wang, Jiliang
Protective Role of mTOR in Liver Ischemia/Reperfusion Injury: Involvement of Inflammation and Autophagy
title Protective Role of mTOR in Liver Ischemia/Reperfusion Injury: Involvement of Inflammation and Autophagy
title_full Protective Role of mTOR in Liver Ischemia/Reperfusion Injury: Involvement of Inflammation and Autophagy
title_fullStr Protective Role of mTOR in Liver Ischemia/Reperfusion Injury: Involvement of Inflammation and Autophagy
title_full_unstemmed Protective Role of mTOR in Liver Ischemia/Reperfusion Injury: Involvement of Inflammation and Autophagy
title_short Protective Role of mTOR in Liver Ischemia/Reperfusion Injury: Involvement of Inflammation and Autophagy
title_sort protective role of mtor in liver ischemia/reperfusion injury: involvement of inflammation and autophagy
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6885218/
https://www.ncbi.nlm.nih.gov/pubmed/31827701
http://dx.doi.org/10.1155/2019/7861290
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