Inflammasomes: sensors of metabolic stresses for vascular inflammation

Yang, Xiao-feng

doi:10.2741/4127

Cited by 134Inflammasome and immune disordersAdipokines, Inflammation, and Metabolic DiseasesAtherosclerosis and Cardiovascular Diseases

Inflammasomes: sensors of metabolic stresses for vascular inflammation

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Yang, Xiao-feng·2013·Frontiers in Bioscience

DOI 10.2741/4127PMC PMC3590813

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Abstract

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.

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The NLRP3 inflammasome plays a central role in the pathogenesis of vascular inflammation.
“Studies have established a central role of nucleotide‐binding oligomerization domain–like receptor family pyrin domain–containing 3 (NLRP3) inflammasome in the pathogenesis of vascular inflammation.”
From Trimethylamine‐N‐Oxide Induces Vascular Inflammation by Activating the NLRP3 Inflammasome Through the SIRT3‐SOD2‐mtROS Signaling Pathway (2017) · cites this paper as [9]
The NLRP3 inflammasome plays a key role in the pathogenesis of diverse inflammatory diseases, including atherosclerosis, type 2 diabetes mellitus, and gout.
“The NLRP3 inflammasome plays a key role in the pathogenesis of diverse inflammatory diseases, including AS, type 2 diabetes mellitus, and gout.9”
From Trimethylamine‐N‐Oxide Induces Vascular Inflammation by Activating the NLRP3 Inflammasome Through the SIRT3‐SOD2‐mtROS Signaling Pathway (2017) · cites this paper as [9]
Oxidized low-density lipoprotein and cholesterol crystals activate the NLRP3 inflammasome, leading to processing and secretion of IL-1β and IL-18 and triggering vascular inflammation via upregulation of adhesion molecules.
“Oxidized low‐density lipoprotein and cholesterol crystals activate the inflammasome, thereby leading to the processing and secretion of the proinflammatory cytokines IL‐1β and IL‐18 and ultimately triggering vascular inflammation via upregulation of adhesion molecules.9, 10”
From Trimethylamine‐N‐Oxide Induces Vascular Inflammation by Activating the NLRP3 Inflammasome Through the SIRT3‐SOD2‐mtROS Signaling Pathway (2017) · cites this paper as [9]
Several endogenous metabolic stress molecules (e.g., oligomers of islet amyloid polypeptide, glucose, ceramid, oxidized LDL, cholesterol crystals) are sensed by NLRP3, stimulating NLRP3 inflammasome complex assembly, leading to activation of caspase-1 and processing/secretion of IL-1β and IL-18.
“Several endogenous metabolic stress molecules, such as oligomers of islet amyloid polypeptide, glucose, ceramid, oxidized LDL, and cholesterol crystals, are sensed by NLRP3, stimulating NLRP3 inflammasome complex assembly and, in turn, leading to activation of caspase‐1 and ultimately to the processing and secretion of the proinflammatory cytokines IL‐1β and IL‐18.9”
From Trimethylamine‐N‐Oxide Induces Vascular Inflammation by Activating the NLRP3 Inflammasome Through the SIRT3‐SOD2‐mtROS Signaling Pathway (2017) · cites this paper as [9]

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[41]Saha N Moldovan F Tardif G Pelletier JP Cloutier JM Martel-Pelletier J Interleukin-1beta-converting enzyme/caspase-1 in human osteoarthritic tissues: localization and role in the maturation of interleukin-1beta and interleukin-18 Arthritis Rheum 1999 42 1577 1587 10446854
[78]Duewell P Kono H Rayner KJ Sirois CM Vladimer G Bauernfeind FG Abela GS Franchi L Nunez G Schnurr M Espevik T Lien E Fitzgerald KA Rock KL Moore KJ Wright SD Hornung V Latz E NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals Nature 2010 464 1357 1361 20428172 PMC2946640

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Authors: Yang, X.-F.
Affiliations: Cardiovascular Research Center (BR)
Corresponding author: Yang, Xiao-feng
Venue: Frontiers in Bioscience
Publisher: IMR Press
Published: 2013
Volume: 18
Issue: 2
Pages: 638
ISSN: 1093-4715 (ISSN-L)
1093-9946
DOI: 10.2741/4127
PMC: PMC3590813
OpenAlex: W2971515230
Cited by: 134
References: 84
Citations by year: 2026: 8 · 2025: 2 · 2024: 9 · 2023: 8 · 2022: 11 · 2021: 10 · 2020: 12 · 2019: 9 · 2018: 11 · 2017: 14 · 2016: 10 · 2015: 7 · 2014: 17 · 2013: 6
FWCI: 0.87
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Frontiers in bioscience (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health
National Heart, Lung, and Blood Institute (HL094451, HL-67033, HL77288, R01HL067033, R01HL117654, HL-108910, R01HL094451, R01HL108910, R01HL110764, R01HL077288, HL-110764)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
Keywords: inflammasome, metabolic stress, vascular inflammation, atherosclerosis, metabolic syndrome, type 2 diabetes, obesity, IL-1β, reactive oxygen species, ion channel models, inflammasome assembly
MeSH terms: NLR Family, Pyrin Domain-Containing 3 Protein, Carrier Proteins, Enzyme Activation, Humans, Inflammation, Stress, Physiological, Reactive Oxygen Species, Caspase 1, Atherosclerosis, Interleukin-1beta, Inflammasomes

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Inflammasomes: sensors of metabolic stresses for vascular inflammation

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