Document Detail


Inflammasomes: sensors of metabolic stresses for vascular inflammation.
MedLine Citation:
PMID:  23276949     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Metabolic syndrome is a major health issue in the western world. An elevated pro-inflammatory state is often found in patients with metabolic diseases such as type 2 diabetes and obesity. Atherosclerosis is one such clinical manifestation of pro-inflammatory state associated with the vasculature. The exact mechanism by which metabolic stress induces this pro-inflammatory status and promotes atherogenesis remained elusive until the discovery of the inflammasome protein complex. This complex is composed of pro-caspase-1 and pathogen sensors. Activation of inflammasome requires the transcriptional upregulation of inflammasome components and the post-translational assembly. Three models of inflammasome assembly have been proposed: 1) the ion channel model; 2) the reactive oxygen species (ROS) model; and 3) the lysosome model. In either case, inflammasome activation triggers the auto-activation of pro-caspase-1 into its mature form. Caspase-1, which was first discovered as the IL-1β converting enzyme, is known to be a major player in inflammatory and cell death pathways. Many endogenous metabolic ligands have been experimentally shown to activate inflammasome, and thus initiate the subsequent inflammation process. Further understanding of the distinct molecular mechanism by which metabolic ligands activates inflammasome could lead to developing novel therapeutic interventions for atherosclerosis and other clinical problems related to metabolic diseases.
Authors:
Ying Yin; Jahaira Lopez Pastrana; Xinyuan Li; Xiao Huang; Karthik Mallilankaraman; Eric T Choi; Muniswamy Madesh; Hong Wang; Xiao-Feng Yang
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review     Date:  2013-01-01
Journal Detail:
Title:  Frontiers in bioscience (Landmark edition)     Volume:  18     ISSN:  1093-4715     ISO Abbreviation:  Front Biosci (Landmark Ed)     Publication Date:  2013  
Date Detail:
Created Date:  2013-01-01     Completed Date:  2013-06-12     Revised Date:  2014-04-10    
Medline Journal Info:
Nlm Unique ID:  101612996     Medline TA:  Front Biosci (Landmark Ed)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  638-49     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Atherosclerosis / etiology
Carrier Proteins / physiology
Caspase 1 / metabolism*
Enzyme Activation
Humans
Inflammasomes / drug effects,  physiology*
Inflammation / etiology*
Interleukin-1beta / metabolism
Reactive Oxygen Species / pharmacology
Stress, Physiological / physiology*
Grant Support
ID/Acronym/Agency:
HL094451/HL/NHLBI NIH HHS; HL108910/HL/NHLBI NIH HHS; HL110764/HL/NHLBI NIH HHS; HL67033/HL/NHLBI NIH HHS; HL77288/HL/NHLBI NIH HHS; R01 HL077288/HL/NHLBI NIH HHS; R01 HL094451/HL/NHLBI NIH HHS; R01 HL108910/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Carrier Proteins; 0/Inflammasomes; 0/Interleukin-1beta; 0/NLRP3 protein, human; 0/Reactive Oxygen Species; EC 3.4.22.36/Caspase 1
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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