Cargando…
Roles of Oxidative Stress, Apoptosis, PGC-1α and Mitochondrial Biogenesis in Cerebral Ischemia
The primary physiological function of mitochondria is to generate adenosine triphosphate through oxidative phosphorylation via the electron transport chain. Overproduction of reactive oxygen species (ROS) as byproducts generated from mitochondria have been implicated in acute brain injuries such as...
Autores principales: | , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Molecular Diversity Preservation International (MDPI)
2011
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3211033/ https://www.ncbi.nlm.nih.gov/pubmed/22072942 http://dx.doi.org/10.3390/ijms12107199 |
_version_ | 1782215794779750400 |
---|---|
author | Chen, Shang-Der Yang, Ding-I Lin, Tsu-Kung Shaw, Fu-Zen Liou, Chia-Wei Chuang, Yao-Chung |
author_facet | Chen, Shang-Der Yang, Ding-I Lin, Tsu-Kung Shaw, Fu-Zen Liou, Chia-Wei Chuang, Yao-Chung |
author_sort | Chen, Shang-Der |
collection | PubMed |
description | The primary physiological function of mitochondria is to generate adenosine triphosphate through oxidative phosphorylation via the electron transport chain. Overproduction of reactive oxygen species (ROS) as byproducts generated from mitochondria have been implicated in acute brain injuries such as stroke from cerebral ischemia. It was well-documented that mitochondria-dependent apoptotic pathway involves pro- and anti-apoptotic protein binding, release of cytochrome c, leading ultimately to neuronal death. On the other hand, mitochondria also play a role to counteract the detrimental effects elicited by excessive oxidative stress. Recent studies have revealed that oxidative stress and the redox state of ischemic neurons are also implicated in the signaling pathway that involves peroxisome proliferative activated receptor-γ (PPARγ) co-activator 1α (PGC1-α). PGC1-α is a master regulator of ROS scavenging enzymes including manganese superoxide dismutase 2 and the uncoupling protein 2, both are mitochondrial proteins, and may contribute to neuronal survival. PGC1-α is also involved in mitochondrial biogenesis that is vital for cell survival. Experimental evidence supports the roles of mitochondrial dysfunction and oxidative stress as determinants of neuronal death as well as endogenous protective mechanisms after stroke. This review aims to summarize the current knowledge focusing on the molecular mechanisms underlying cerebral ischemia involving ROS, mitochondrial dysfunction, apoptosis, mitochondrial proteins capable of ROS scavenging, and mitochondrial biogenesis. |
format | Online Article Text |
id | pubmed-3211033 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | Molecular Diversity Preservation International (MDPI) |
record_format | MEDLINE/PubMed |
spelling | pubmed-32110332011-11-09 Roles of Oxidative Stress, Apoptosis, PGC-1α and Mitochondrial Biogenesis in Cerebral Ischemia Chen, Shang-Der Yang, Ding-I Lin, Tsu-Kung Shaw, Fu-Zen Liou, Chia-Wei Chuang, Yao-Chung Int J Mol Sci Review The primary physiological function of mitochondria is to generate adenosine triphosphate through oxidative phosphorylation via the electron transport chain. Overproduction of reactive oxygen species (ROS) as byproducts generated from mitochondria have been implicated in acute brain injuries such as stroke from cerebral ischemia. It was well-documented that mitochondria-dependent apoptotic pathway involves pro- and anti-apoptotic protein binding, release of cytochrome c, leading ultimately to neuronal death. On the other hand, mitochondria also play a role to counteract the detrimental effects elicited by excessive oxidative stress. Recent studies have revealed that oxidative stress and the redox state of ischemic neurons are also implicated in the signaling pathway that involves peroxisome proliferative activated receptor-γ (PPARγ) co-activator 1α (PGC1-α). PGC1-α is a master regulator of ROS scavenging enzymes including manganese superoxide dismutase 2 and the uncoupling protein 2, both are mitochondrial proteins, and may contribute to neuronal survival. PGC1-α is also involved in mitochondrial biogenesis that is vital for cell survival. Experimental evidence supports the roles of mitochondrial dysfunction and oxidative stress as determinants of neuronal death as well as endogenous protective mechanisms after stroke. This review aims to summarize the current knowledge focusing on the molecular mechanisms underlying cerebral ischemia involving ROS, mitochondrial dysfunction, apoptosis, mitochondrial proteins capable of ROS scavenging, and mitochondrial biogenesis. Molecular Diversity Preservation International (MDPI) 2011-10-21 /pmc/articles/PMC3211033/ /pubmed/22072942 http://dx.doi.org/10.3390/ijms12107199 Text en © 2011 by the authors; licensee MDPI, Basel, Switzerland. http://creativecommons.org/licenses/by/3.0 This article is an open-access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/). |
spellingShingle | Review Chen, Shang-Der Yang, Ding-I Lin, Tsu-Kung Shaw, Fu-Zen Liou, Chia-Wei Chuang, Yao-Chung Roles of Oxidative Stress, Apoptosis, PGC-1α and Mitochondrial Biogenesis in Cerebral Ischemia |
title | Roles of Oxidative Stress, Apoptosis, PGC-1α and Mitochondrial Biogenesis in Cerebral Ischemia |
title_full | Roles of Oxidative Stress, Apoptosis, PGC-1α and Mitochondrial Biogenesis in Cerebral Ischemia |
title_fullStr | Roles of Oxidative Stress, Apoptosis, PGC-1α and Mitochondrial Biogenesis in Cerebral Ischemia |
title_full_unstemmed | Roles of Oxidative Stress, Apoptosis, PGC-1α and Mitochondrial Biogenesis in Cerebral Ischemia |
title_short | Roles of Oxidative Stress, Apoptosis, PGC-1α and Mitochondrial Biogenesis in Cerebral Ischemia |
title_sort | roles of oxidative stress, apoptosis, pgc-1α and mitochondrial biogenesis in cerebral ischemia |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3211033/ https://www.ncbi.nlm.nih.gov/pubmed/22072942 http://dx.doi.org/10.3390/ijms12107199 |
work_keys_str_mv | AT chenshangder rolesofoxidativestressapoptosispgc1aandmitochondrialbiogenesisincerebralischemia AT yangdingi rolesofoxidativestressapoptosispgc1aandmitochondrialbiogenesisincerebralischemia AT lintsukung rolesofoxidativestressapoptosispgc1aandmitochondrialbiogenesisincerebralischemia AT shawfuzen rolesofoxidativestressapoptosispgc1aandmitochondrialbiogenesisincerebralischemia AT liouchiawei rolesofoxidativestressapoptosispgc1aandmitochondrialbiogenesisincerebralischemia AT chuangyaochung rolesofoxidativestressapoptosispgc1aandmitochondrialbiogenesisincerebralischemia |