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The NLRP3 inflammasome: a sensor for metabolic danger?Schroder K; Zhou R; Tschopp JScience 2010[Jan]; 327 (5963): 296-300Interleukin-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.|*Inflammation[MESH]|*Stress, Physiological[MESH]|Animals[MESH]|Carrier Proteins/*metabolism[MESH]|Diabetes Mellitus, Type 2/immunology/*metabolism/physiopathology[MESH]|Gout/immunology/metabolism[MESH]|Humans[MESH]|Insulin-Secreting Cells/physiology[MESH]|Interleukin-1beta/metabolism[MESH]|Multiprotein Complexes/*metabolism[MESH]|NLR Family, Pyrin Domain-Containing 3 Protein[MESH]|Reactive Oxygen Species/metabolism[MESH] |
