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巨噬细胞中的 NLRP3 和 IL-1β 作为代谢疾病的关键调节因子。

NLRP3 and IL-1β in macrophages as critical regulators of metabolic diseases.

机构信息

School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland.

出版信息

Diabetes Obes Metab. 2013 Sep;15 Suppl 3:19-25. doi: 10.1111/dom.12169.

Abstract

The activation of the NLRP3 inflammasome leads to the autocleavage and activation of caspase-1. Caspase-1 cleaves several substrates, including the pro-inflammatory cytokine IL-1β. Inflammation, in particular IL-1β, has long been associated with the progression of metabolic disorders, and recent evidence suggests that the NLRP3 inflammasome plays a critical role in this inflammation. This review concentrates on the activation of NLRP3 during the development of metabolic disorders and the effect this activation has on the inflammatory state as well as the metabolic state of the cell.

摘要

NLRP3 炎性小体的激活导致半胱天冬酶-1 的自身切割和激活。半胱天冬酶-1 切割几种底物,包括促炎细胞因子 IL-1β。炎症,特别是 IL-1β,长期以来一直与代谢紊乱的进展有关,最近的证据表明 NLRP3 炎性小体在这种炎症中起着关键作用。本综述集中讨论了 NLRP3 在代谢紊乱发展过程中的激活及其对细胞炎症状态和代谢状态的影响。

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