The nod-like receptor protein 3 (NLRP3) inflammasome drives inflammation in response to mitochondrial dysfunction. As metabolic powerhouses with prokaryotic ancestry, mitochondria are a cache for danger-associated molecular patterns and pathogen-associated molecular pattern-like molecules that elicit potent innate immune responses. Persistent mitochondrial damage caused by infection, or genetic or environmental factors, can lead to inappropriate or sustained inflammasome signalling. Here, we review the features of mitochondria that drive inflammatory signalling, with a particular focus on mitochondrial activation of the NLRP3 inflammasome. Given that mitochondrial network dynamics, metabolic activity and redox state are all intricately linked to each other and to NLRP3 inflammasome activity, we highlight the importance of a holistic approach to investigations of NLRP3 activation by dysfunctional mitochondria.

中文翻译：

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炎症的rOX明星：炎症小体与线粒体融化之间的联系。

点状受体蛋白3（NLRP3）炎症小体响应线粒体功能障碍而驱动炎症。线粒体作为具有原核祖先的代谢强国，是引发潜在的先天免疫反应的危险相关分子模式和病原体相关分子模式样分子的缓存区。由感染或遗传或环境因素引起的持续性线粒体损害可导致不适当或持续的炎症信号。在这里，我们审查了线粒体驱动炎症信号的特征，特别是线粒体激活NLRP3炎性体的研究。鉴于线粒体网络动态，代谢活性和氧化还原状态都彼此之间以及与NLRP3炎症小体活性之间有着千丝万缕的联系，