The University of Queensland, Institute for Molecular Bioscience, 4072 Brisbane, Australia.
The University of Queensland, Centre for Microscopy and Microanalysis, 4072 Brisbane, Australia.
Biochem Soc Trans. 2023 Jun 28;51(3):1377-1385. doi: 10.1042/BST20230121.
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.
氧化应激是许多疾病的特征。氧化应激可以激活许多导致细胞死亡的细胞途径,包括一种涉及脂质过氧化的独特的铁依赖性途径,称为铁死亡,但细胞已经进化出复杂的机制来应对这些应激。在这里,我们简要总结了目前将 caveolae 与细胞氧化应激反应联系起来的证据。我们讨论了最近在培养细胞和体内模型中的研究,表明氧化应激驱动的脂质过氧化导致 caveolae 的解体,将 caveola 蛋白释放到细胞中,在那里它们调节转录主控制器,红细胞生成 2 相关因子 2。这些研究表明 caveolae 维持细胞对氧化应激诱导的细胞死亡的敏感性,并表明其在细胞内稳态和对创伤的反应中起着至关重要的作用。