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

被引：59

作者：

McGettrick, A. F. ^{[1
]}

O'Neill, L. A. J. ^{[1
]}

机构：

[1] Trinity Coll Dublin, Trinity Biomed Sci Inst, Sch Biochem & Immunol, Dublin 2, Ireland

来源：

DIABETES OBESITY & METABOLISM | 2013年 / 15卷

基金：

爱尔兰科学基金会; 欧洲研究理事会;

关键词：

AMPK; glycolysis; inflammasome; metabolic disorders; NLRP3; ACTIVATED PROTEIN-KINASE; TYPE-2; DIABETES-MELLITUS; INSULIN-RESISTANCE; NALP3; INFLAMMASOME; ADIPOSE-TISSUE; OXIDATIVE STRESS; SKELETAL-MUSCLE; DANGER SIGNAL; SIRT1; CRYSTALS;

D O I：

10.1111/dom.12169

中图分类号：

R5 [内科学];

学科分类号：

100201 [内科学];

摘要：

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-1 beta. Inflammation, in particular IL-1 beta, 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.

引用

页码：19 / 25

页数：7

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