Inflammasornes and Metabolic Disorders: Old Genes in Modern Diseases

被引:93
作者
Robbins, Gregory R. [1 ,2 ]
Wen, Haitao [1 ,3 ]
Ting, Jenny P. -Y. [1 ,2 ]
机构
[1] Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA
[2] Univ N Carolina, Dept Microbiol & Immunol, Chapel Hill, NC 27599 USA
[3] Univ N Carolina, Dept Surg, Chapel Hill, NC 27599 USA
关键词
INTERLEUKIN-1 RECEPTOR ANTAGONIST; THIOREDOXIN-INTERACTING PROTEIN; PATTERN-RECOGNITION RECEPTORS; ENDOPLASMIC-RETICULUM STRESS; ISLET AMYLOID POLYPEPTIDE; NLRP3; INFLAMMASOME; CELL-DEATH; VASCULAR INFLAMMATION; CASPASE-1; ACTIVATION; INSULIN-RESISTANCE;
D O I
10.1016/j.molcel.2014.03.029
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
Modern medical and hygienic practices have greatly improved human health and longevity; however, increased human life span occurs concomitantly with the emergence of metabolic and age-related diseases. Studies over the past decade have strongly linked host inflammatory responses to the etiology of several metabolic diseases including atherosclerosis, type 2 diabetes (T2D), obesity, and gout. A common immunological factor to these diseases is the activation of the inflammasome and release of proinflammatory cytokines that promote disease progression. Here we review the molecular mechanism(s) of inflammasome activation in response to metabolic damage-associated molecular patterns (DAMPs) and discuss potential targets for therapeutic intervention.
引用
收藏
页码:297 / 308
页数:12
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