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Mitochondrial Dysfunction and Autophagy in Hepatic Ischemia/Reperfusion Injury

Ischemia/reperfusion (I/R) injury remains a major complication of liver resection, transplantation, and hemorrhagic shock. Although the mechanisms that contribute to hepatic I/R are complex and diverse involving the interaction of cell injury in hepatocytes, immune cells, and endothelium, mitochondr...

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Autores principales: Go, Kristina L., Lee, Sooyeon, Zendejas, Ivan, Behrns, Kevin E., Kim, Jae-Sung
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4684839/
https://www.ncbi.nlm.nih.gov/pubmed/26770970
http://dx.doi.org/10.1155/2015/183469
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author Go, Kristina L.
Lee, Sooyeon
Zendejas, Ivan
Behrns, Kevin E.
Kim, Jae-Sung
author_facet Go, Kristina L.
Lee, Sooyeon
Zendejas, Ivan
Behrns, Kevin E.
Kim, Jae-Sung
author_sort Go, Kristina L.
collection PubMed
description Ischemia/reperfusion (I/R) injury remains a major complication of liver resection, transplantation, and hemorrhagic shock. Although the mechanisms that contribute to hepatic I/R are complex and diverse involving the interaction of cell injury in hepatocytes, immune cells, and endothelium, mitochondrial dysfunction is a cardinal event culminating in hepatic reperfusion injury. Mitochondrial autophagy, so-called mitophagy, is a key cellular process that regulates mitochondrial homeostasis and eliminates damaged mitochondria in a timely manner. Growing evidence accumulates that I/R injury is attributed to defective mitophagy. This review aims to summarize the current understanding of autophagy and its role in hepatic I/R injury and highlight the various therapeutic approaches that have been studied to ameliorate injury.
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spelling pubmed-46848392016-01-14 Mitochondrial Dysfunction and Autophagy in Hepatic Ischemia/Reperfusion Injury Go, Kristina L. Lee, Sooyeon Zendejas, Ivan Behrns, Kevin E. Kim, Jae-Sung Biomed Res Int Review Article Ischemia/reperfusion (I/R) injury remains a major complication of liver resection, transplantation, and hemorrhagic shock. Although the mechanisms that contribute to hepatic I/R are complex and diverse involving the interaction of cell injury in hepatocytes, immune cells, and endothelium, mitochondrial dysfunction is a cardinal event culminating in hepatic reperfusion injury. Mitochondrial autophagy, so-called mitophagy, is a key cellular process that regulates mitochondrial homeostasis and eliminates damaged mitochondria in a timely manner. Growing evidence accumulates that I/R injury is attributed to defective mitophagy. This review aims to summarize the current understanding of autophagy and its role in hepatic I/R injury and highlight the various therapeutic approaches that have been studied to ameliorate injury. Hindawi Publishing Corporation 2015 2015-12-06 /pmc/articles/PMC4684839/ /pubmed/26770970 http://dx.doi.org/10.1155/2015/183469 Text en Copyright © 2015 Kristina L. Go et al. https://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
Go, Kristina L.
Lee, Sooyeon
Zendejas, Ivan
Behrns, Kevin E.
Kim, Jae-Sung
Mitochondrial Dysfunction and Autophagy in Hepatic Ischemia/Reperfusion Injury
title Mitochondrial Dysfunction and Autophagy in Hepatic Ischemia/Reperfusion Injury
title_full Mitochondrial Dysfunction and Autophagy in Hepatic Ischemia/Reperfusion Injury
title_fullStr Mitochondrial Dysfunction and Autophagy in Hepatic Ischemia/Reperfusion Injury
title_full_unstemmed Mitochondrial Dysfunction and Autophagy in Hepatic Ischemia/Reperfusion Injury
title_short Mitochondrial Dysfunction and Autophagy in Hepatic Ischemia/Reperfusion Injury
title_sort mitochondrial dysfunction and autophagy in hepatic ischemia/reperfusion injury
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4684839/
https://www.ncbi.nlm.nih.gov/pubmed/26770970
http://dx.doi.org/10.1155/2015/183469
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