Inflammation driven by the NLRP3 inflammasome in macrophages is an important contributor to chronic metabolic diseases that affect growing numbers of individuals. Many of these diseases involve the pathologic accumulation of endogenous lipids or their oxidation products, which can activate NLRP3. Other endogenous lipids, however, can inhibit the activation of NLRP3. The intracellular mechanisms by which these lipids modulate NLRP3 activity are now being identified. This review discusses emerging evidence suggesting that organelle stress, particularly involving mitochondria, lysosomes, and the endoplasmic reticulum, may be key in lipid-induced modification of NLRP3 inflammasome activity.

由巨噬细胞中的 NLRP3 炎性体驱动的炎症是影响越来越多个体的慢性代谢疾病的重要原因。许多这些疾病涉及内源性脂质或其氧化产物的病理性积累，它们可以激活 NLRP3。然而，其他内源性脂质可以抑制 NLRP3 的激活。现在正在确定这些脂质调节 NLRP3 活性的细胞内机制。这篇综述讨论了新出现的证据，这些证据表明细胞器应激，特别是涉及线粒体、溶酶体和内质网，可能是脂质诱导的 NLRP3 炎性体活性修饰的关键。