The NLRP3 inflammasome: a sensor for metabolic danger?

Schroder, Kate, Zhou, Rongbin and Tschopp, Jurg (2010) The NLRP3 inflammasome: a sensor for metabolic danger?. Science, 327 5963: 269-300. doi:10.1126/science.1184003


Author Schroder, Kate
Zhou, Rongbin
Tschopp, Jurg
Title The NLRP3 inflammasome: a sensor for metabolic danger?
Journal name Science   Check publisher's open access policy
ISSN 1095-9203
0036-8075
Publication date 2010-01-15
Year available 2010
Sub-type Article (original research)
DOI 10.1126/science.1184003
Volume 327
Issue 5963
Start page 269
End page 300
Total pages 32
Place of publication Washington, DC, U.S.A.
Publisher American Association for the Advancement of Science
Collection year 2011
Language eng
Abstract Interleukin-1β (IL-1β), 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-1β production and its pathogenic role in islet dysfunction during chronic hyperglycemia. In doing so, we integrate previously disparate disease-driving mechanisms for IL-1β, ROS, and TXNIP in T2DM into one unifying model in which the NLRP3 inflammasome plays a central role. The NLRP3 inflammasome also drives IL-1β 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.
Keyword Beta-cell apoptosis
Thioredoxin-interacting protein
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Non HERDC
Institute for Molecular Bioscience - Publications
 
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Created: Wed, 02 Feb 2011, 17:15:04 EST by Dr Kate Schroder on behalf of Institute for Molecular Bioscience