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Role of Mitochondrial Pathways in Cell Apoptosis during He-Patic Ischemia/Reperfusion Injury

Hepatic ischemia-reperfusion injury is a major cause of post-operative hepatic dysfunction and liver failure after transplantation. Mitochondrial pathways can be either beneficial or detrimental to hepatic cell apoptosis during hepatic ischemia/reperfusion injury, depending on multiple factors. Hepa...

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Detalles Bibliográficos
Autores principales: Zhang, Sen, Rao, Sijing, Yang, Meiwen, Ma, Chen, Hong, Fengfang, Yang, Shulong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8877300/
https://www.ncbi.nlm.nih.gov/pubmed/35216473
http://dx.doi.org/10.3390/ijms23042357
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author Zhang, Sen
Rao, Sijing
Yang, Meiwen
Ma, Chen
Hong, Fengfang
Yang, Shulong
author_facet Zhang, Sen
Rao, Sijing
Yang, Meiwen
Ma, Chen
Hong, Fengfang
Yang, Shulong
author_sort Zhang, Sen
collection PubMed
description Hepatic ischemia-reperfusion injury is a major cause of post-operative hepatic dysfunction and liver failure after transplantation. Mitochondrial pathways can be either beneficial or detrimental to hepatic cell apoptosis during hepatic ischemia/reperfusion injury, depending on multiple factors. Hepatic ischemia/reperfusion injury may be induced by opened mitochondrial permeability transition pore, released apoptosis-related proteins, up-regulated B-cell lymphoma-2 gene family proteins, unbalanced mitochondrial dynamics, and endoplasmic reticulum stress, which are integral parts of mitochondrial pathways. In this review, we discuss the role of mitochondrial pathways in apoptosis that account for the most deleterious effect of hepatic ischemia/reperfusion injury.
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spelling pubmed-88773002022-02-26 Role of Mitochondrial Pathways in Cell Apoptosis during He-Patic Ischemia/Reperfusion Injury Zhang, Sen Rao, Sijing Yang, Meiwen Ma, Chen Hong, Fengfang Yang, Shulong Int J Mol Sci Review Hepatic ischemia-reperfusion injury is a major cause of post-operative hepatic dysfunction and liver failure after transplantation. Mitochondrial pathways can be either beneficial or detrimental to hepatic cell apoptosis during hepatic ischemia/reperfusion injury, depending on multiple factors. Hepatic ischemia/reperfusion injury may be induced by opened mitochondrial permeability transition pore, released apoptosis-related proteins, up-regulated B-cell lymphoma-2 gene family proteins, unbalanced mitochondrial dynamics, and endoplasmic reticulum stress, which are integral parts of mitochondrial pathways. In this review, we discuss the role of mitochondrial pathways in apoptosis that account for the most deleterious effect of hepatic ischemia/reperfusion injury. MDPI 2022-02-21 /pmc/articles/PMC8877300/ /pubmed/35216473 http://dx.doi.org/10.3390/ijms23042357 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Zhang, Sen
Rao, Sijing
Yang, Meiwen
Ma, Chen
Hong, Fengfang
Yang, Shulong
Role of Mitochondrial Pathways in Cell Apoptosis during He-Patic Ischemia/Reperfusion Injury
title Role of Mitochondrial Pathways in Cell Apoptosis during He-Patic Ischemia/Reperfusion Injury
title_full Role of Mitochondrial Pathways in Cell Apoptosis during He-Patic Ischemia/Reperfusion Injury
title_fullStr Role of Mitochondrial Pathways in Cell Apoptosis during He-Patic Ischemia/Reperfusion Injury
title_full_unstemmed Role of Mitochondrial Pathways in Cell Apoptosis during He-Patic Ischemia/Reperfusion Injury
title_short Role of Mitochondrial Pathways in Cell Apoptosis during He-Patic Ischemia/Reperfusion Injury
title_sort role of mitochondrial pathways in cell apoptosis during he-patic ischemia/reperfusion injury
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8877300/
https://www.ncbi.nlm.nih.gov/pubmed/35216473
http://dx.doi.org/10.3390/ijms23042357
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