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Caveolae and the oxidative stress response

Oxidative stress is a feature of many disease conditions. Oxidative stress can activate a number of cellular pathways leading to cell death, including a distinct iron-dependent pathway involving lipid peroxidation, termed ferroptosis, but cells have evolved complex mechanisms to respond to these str...

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Detalles Bibliográficos
Autores principales: Wu, Yeping, Lim, Ye-Wheen, Parton, Robert G.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Portland Press Ltd. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10317157/
https://www.ncbi.nlm.nih.gov/pubmed/37248872
http://dx.doi.org/10.1042/BST20230121
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author Wu, Yeping
Lim, Ye-Wheen
Parton, Robert G.
author_facet Wu, Yeping
Lim, Ye-Wheen
Parton, Robert G.
author_sort Wu, Yeping
collection PubMed
description Oxidative stress is a feature of many disease conditions. Oxidative stress can activate a number of cellular pathways leading to cell death, including a distinct iron-dependent pathway involving lipid peroxidation, termed ferroptosis, but cells have evolved complex mechanisms to respond to these stresses. Here, we briefly summarise current evidence linking caveolae to the cellular oxidative stress response. We discuss recent studies in cultured cells and in an in vivo model suggesting that lipid peroxidation driven by oxidative stress causes disassembly of caveolae to release caveola proteins into the cell where they regulate the master transcriptional redox controller, nuclear factor erythroid 2-related factor 2. These studies suggest that caveolae maintain cellular susceptibility to oxidative stress-induced cell death and suggest a crucial role in cellular homeostasis and the response to wounding.
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spelling pubmed-103171572023-07-04 Caveolae and the oxidative stress response Wu, Yeping Lim, Ye-Wheen Parton, Robert G. Biochem Soc Trans Review Articles Oxidative stress is a feature of many disease conditions. Oxidative stress can activate a number of cellular pathways leading to cell death, including a distinct iron-dependent pathway involving lipid peroxidation, termed ferroptosis, but cells have evolved complex mechanisms to respond to these stresses. Here, we briefly summarise current evidence linking caveolae to the cellular oxidative stress response. We discuss recent studies in cultured cells and in an in vivo model suggesting that lipid peroxidation driven by oxidative stress causes disassembly of caveolae to release caveola proteins into the cell where they regulate the master transcriptional redox controller, nuclear factor erythroid 2-related factor 2. These studies suggest that caveolae maintain cellular susceptibility to oxidative stress-induced cell death and suggest a crucial role in cellular homeostasis and the response to wounding. Portland Press Ltd. 2023-06-28 2023-05-30 /pmc/articles/PMC10317157/ /pubmed/37248872 http://dx.doi.org/10.1042/BST20230121 Text en © 2023 The Author(s) https://creativecommons.org/licenses/by/4.0/This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY) (https://creativecommons.org/licenses/by/4.0/) . Open access for this article was enabled by the participation of the University of Queensland in an all-inclusive Read & Publish agreement with Portland Press and the Biochemical Society under a transformative agreement with CAUL.
spellingShingle Review Articles
Wu, Yeping
Lim, Ye-Wheen
Parton, Robert G.
Caveolae and the oxidative stress response
title Caveolae and the oxidative stress response
title_full Caveolae and the oxidative stress response
title_fullStr Caveolae and the oxidative stress response
title_full_unstemmed Caveolae and the oxidative stress response
title_short Caveolae and the oxidative stress response
title_sort caveolae and the oxidative stress response
topic Review Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10317157/
https://www.ncbi.nlm.nih.gov/pubmed/37248872
http://dx.doi.org/10.1042/BST20230121
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