The Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA; Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
The Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA; Department of Surgery, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Mol Cell. 2014 Apr 24;54(2):297-308. doi: 10.1016/j.molcel.2014.03.029.
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.
现代医学和卫生实践极大地提高了人类的健康和寿命；然而，人类寿命的延长伴随着代谢和与年龄相关的疾病的出现。过去十年的研究强烈表明，宿主炎症反应与几种代谢疾病（包括动脉粥样硬化、2 型糖尿病（T2D）、肥胖症和痛风）的病因有关。这些疾病的一个共同的免疫学因素是炎症小体的激活和促炎细胞因子的释放，促进疾病的进展。在这里，我们回顾了炎症小体对代谢损伤相关分子模式（DAMPs）的激活的分子机制，并讨论了潜在的治疗干预靶点。
