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      The NLRP3 inflammasome: a sensor for metabolic danger?

      Science (New York, N.Y.)

      Animals, Carrier Proteins, metabolism, Diabetes Mellitus, Type 2, immunology, physiopathology, Gout, Humans, Inflammation, Insulin-Secreting Cells, physiology, Interleukin-1beta, secretion, Multiprotein Complexes, Reactive Oxygen Species, Stress, Physiological

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          Abstract

          Interleukin-1beta (IL-1beta), reactive oxygen species (ROS), and thioredoxin-interacting protein (TXNIP) are all implicated in the pathogenesis of type 2 diabetes mellitus (T2DM). Here we review mechanisms directing IL-1beta production and its pathogenic role in islet dysfunction during chronic hyperglycemia. In doing so, we integrate previously disparate disease-driving mechanisms for IL-1beta, ROS, and TXNIP in T2DM into one unifying model in which the NLRP3 inflammasome plays a central role. The NLRP3 inflammasome also drives IL-1beta maturation and secretion in another disease of metabolic dysregulation, gout. Thus, we propose that the NLRP3 inflammasome contributes to the pathogenesis of T2DM and gout by functioning as a sensor for metabolic stress.

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          Journal
          20075245
          10.1126/science.1184003

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