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Mitochondrial Stress Signaling Promotes Cellular Adaptations

Mitochondrial dysfunction has been implicated in the aetiology of many complex diseases, as well as the ageing process. Much of the research on mitochondrial dysfunction has focused on how mitochondrial damage may potentiate pathological phenotypes. The purpose of this review is to draw attention to...

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Detalles Bibliográficos
Autores principales: Barbour, Jayne Alexandra, Turner, Nigel
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3920668/
https://www.ncbi.nlm.nih.gov/pubmed/24587804
http://dx.doi.org/10.1155/2014/156020
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author Barbour, Jayne Alexandra
Turner, Nigel
author_facet Barbour, Jayne Alexandra
Turner, Nigel
author_sort Barbour, Jayne Alexandra
collection PubMed
description Mitochondrial dysfunction has been implicated in the aetiology of many complex diseases, as well as the ageing process. Much of the research on mitochondrial dysfunction has focused on how mitochondrial damage may potentiate pathological phenotypes. The purpose of this review is to draw attention to the less well-studied mechanisms by which the cell adapts to mitochondrial perturbations. This involves communication of stress to the cell and successful induction of quality control responses, which include mitophagy, unfolded protein response, upregulation of antioxidant and DNA repair enzymes, morphological changes, and if all else fails apoptosis. The mitochondrion is an inherently stressful environment and we speculate that dysregulation of stress signaling or an inability to switch on these adaptations during times of mitochondrial stress may underpin mitochondrial dysfunction and hence amount to pathological states over time.
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spelling pubmed-39206682014-03-02 Mitochondrial Stress Signaling Promotes Cellular Adaptations Barbour, Jayne Alexandra Turner, Nigel Int J Cell Biol Review Article Mitochondrial dysfunction has been implicated in the aetiology of many complex diseases, as well as the ageing process. Much of the research on mitochondrial dysfunction has focused on how mitochondrial damage may potentiate pathological phenotypes. The purpose of this review is to draw attention to the less well-studied mechanisms by which the cell adapts to mitochondrial perturbations. This involves communication of stress to the cell and successful induction of quality control responses, which include mitophagy, unfolded protein response, upregulation of antioxidant and DNA repair enzymes, morphological changes, and if all else fails apoptosis. The mitochondrion is an inherently stressful environment and we speculate that dysregulation of stress signaling or an inability to switch on these adaptations during times of mitochondrial stress may underpin mitochondrial dysfunction and hence amount to pathological states over time. Hindawi Publishing Corporation 2014 2014-01-22 /pmc/articles/PMC3920668/ /pubmed/24587804 http://dx.doi.org/10.1155/2014/156020 Text en Copyright © 2014 J. A. Barbour and N. Turner. https://creativecommons.org/licenses/by/3.0/ 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
Barbour, Jayne Alexandra
Turner, Nigel
Mitochondrial Stress Signaling Promotes Cellular Adaptations
title Mitochondrial Stress Signaling Promotes Cellular Adaptations
title_full Mitochondrial Stress Signaling Promotes Cellular Adaptations
title_fullStr Mitochondrial Stress Signaling Promotes Cellular Adaptations
title_full_unstemmed Mitochondrial Stress Signaling Promotes Cellular Adaptations
title_short Mitochondrial Stress Signaling Promotes Cellular Adaptations
title_sort mitochondrial stress signaling promotes cellular adaptations
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3920668/
https://www.ncbi.nlm.nih.gov/pubmed/24587804
http://dx.doi.org/10.1155/2014/156020
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