Inflammasomes are multi‐protein complexes that regulate the cleavage of cysteine protease caspase‐1, secretion of inflammatory cytokines, and induction of inflammatory cell death, pyroptosis. Several members of the nod‐like receptor family assemble inflammasome in response to specific ligands. An exception to this is the NLRP3 inflammasome which is activated by structurally diverse entities. Recent studies have suggested that NLRP3 might be a sensor of cellular homeostasis, and any perturbation in distinct metabolic pathways results in the activation of this inflammasome. Lipid metabolism is exceedingly important in maintaining cellular homeostasis, and it is recognized that cells and tissues undergo extensive lipid remodeling during activation and disease. Some lipids are involved in instigating chronic inflammatory diseases, and new studies have highlighted critical upstream roles for lipids, particularly cholesterol, in regulating inflammasome activation implying key functions for inflammasomes in diseases with defective lipid metabolism. The focus of this review is to highlight how lipids regulate inflammasome activation and how this leads to the progression of inflammatory diseases. The key roles of cholesterol metabolism in the activation of inflammasomes have been comprehensively discussed. Besides, the roles of oxysterols, fatty acids, phospholipids, and lipid second messengers are also summarized in the context of inflammasomes. The overriding theme is that lipid metabolism has numerous but complex functions in inflammasome activation. A detailed understanding of this area will help us develop therapeutic interventions for diseases where dysregulated lipid metabolism is the underlying cause.

中文翻译：

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脂质、炎症小体、代谢和疾病。

炎性体是多蛋白复合物，可调节半胱氨酸蛋白酶 caspase-1 的裂解、炎性细胞因子的分泌以及诱导炎性细胞死亡、细胞焦亡。nod 样受体家族的几个成员响应特定的配体组装炎性体。一个例外是 NLRP3 炎症小体，它由结构不同的实体激活。最近的研究表明 NLRP3 可能是细胞稳态的传感器，不同代谢途径中的任何扰动都会导致这种炎症小体的激活。脂质代谢在维持细胞稳态方面极其重要，并且公认细胞和组织在活化和疾病期间经历广泛的脂质重塑。一些脂质参与引发慢性炎症疾病，新的研究强调了脂质（尤其是胆固醇）在调节炎症小体激活方面的关键上游作用，这意味着炎症小体在脂质代谢缺陷疾病中的关键功能。本综述的重点是强调脂质如何调节炎症小体激活以及这如何导致炎症疾病的进展。胆固醇代谢在炎症小体激活中的关键作用已得到全面讨论。此外，氧甾醇、脂肪酸、磷脂和脂质第二信使的作用也在炎症小体的背景下进行了总结。压倒一切的主题是脂质代谢在炎症小体激活中具有众多但复杂的功能。