Caveolae and the oxidative stress response

Author:

Wu Yeping1,Lim Ye-Wheen1,Parton Robert G.12ORCID

Affiliation:

1. 1The University of Queensland, Institute for Molecular Bioscience, 4072 Brisbane, Australia

2. 2The University of Queensland, Centre for Microscopy and Microanalysis, 4072 Brisbane, Australia

Abstract

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.

Publisher

Portland Press Ltd.

Subject

Biochemistry

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