Mechanisms of NLRP3 priming in inflammaging and age related diseases

被引：95
作者：
Gritsenko, Anna [1 ]
Green, Jack P. [2 ]
Brough, David [2 ]
Lopez-Castejon, Gloria [1 ]
机构：
[1] Univ Manchester, Manchester Acad Hlth Sci Ctr, Fac Biol Med & Hlth, Lydia Becker Inst Immunol & Inflammat,Div Infect, Manchester, Lancs, England
[2] Univ Manchester, Manchester Acad Hlth Sci Ctr, Fac Biol Med & Hlth, Lydia Becker Inst Immunol & Inflammat,Div Neurosc, Manchester, Lancs, England
来源：
CYTOKINE & GROWTH FACTOR REVIEWS | 2020年 / 55卷
基金：
英国医学研究理事会; 英国惠康基金;
关键词：
NLRP3; Inflammasome; Priming; Inflammaging; Senescence; Aging; MACROPHAGE ACCUMULATION; CELLULAR SENESCENCE; PATTERN-RECOGNITION; SECRETORY PHENOTYPE; NALP3; INFLAMMASOME; P2X(7) RECEPTOR; HUMAN MONOCYTES; ACTIVATION; OBESITY; PROTEIN;
D O I：
10.1016/j.cytogfr.2020.08.003
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
The NLRP3 inflammasome is a vital part of the innate immune response, whilst its aberrant activation drives the progression of a number of non-communicable diseases. Thus, NLRP3 inflammasome assembly must be tightly controlled at several checkpoints. The priming step of NLRP3 inflammasome activation is associated with increased NLRP3 gene expression, as well as post-translational modifications that control NLRP3 levels and licence the NLRP3 protein for inflammasome assembly. Increasing life expectancy in modern society is accompanied by a growing percentage of elderly individuals. The process of aging is associated with chronic inflammation that drives and/or worsens a range of age related non-communicable conditions. The NLRP3 inflammasome is known to contribute to pathological inflammation in many settings, but the mechanisms that prime NLRP3 for activation throughout aging and related co-morbidities have not been extensively reviewed. Here we dissect the biochemical changes that occur during aging and the pathogenesis of age related diseases and analyse the mechanisms by which they prime the NLRP3 inflammasome, thus exacerbating inflammation.
引用
收藏
页码：15 / 25
页数：11
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