通过细胞器应激调节 NLRP3 炎性体活性的脂质。
Lipid regulation of NLRP3 inflammasome activity through organelle stress.
机构信息
Signaling Systems Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Disease (NIAID), National Institutes of Health (NIH), Bethesda, MD, USA; Department of Medicine, University of Cambridge, Cambridge, UK.
Signaling Systems Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Disease (NIAID), National Institutes of Health (NIH), Bethesda, MD, USA.
出版信息
Trends Immunol. 2021 Sep;42(9):807-823. doi: 10.1016/j.it.2021.07.005. Epub 2021 Jul 30.
Abstract
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.
摘要
巨噬细胞中由 NLRP3 炎性小体驱动的炎症是导致越来越多的人患上慢性代谢性疾病的重要因素。这些疾病中有许多涉及内源性脂质或其氧化产物的病理性积累，这些物质可以激活 NLRP3。然而，其他内源性脂质也可以抑制 NLRP3 的激活。这些脂质调节 NLRP3 活性的细胞内机制正在被确定。这篇综述讨论了新出现的证据，表明细胞器应激，特别是涉及线粒体、溶酶体和内质网的应激，可能是脂质诱导 NLRP3 炎性小体活性改变的关键。
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