Evidence map›Paper›PMID 32545355›Full record

ReviewInternational journal of molecular sciences2020

NLRP3 Inflammasome Activation in Adipose Tissues and Its Implications on Metabolic Diseases.

Kelvin Ka-Lok Wu, Samson Wing-Ming Cheung, Kenneth King-Yip Cheng

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
4.1field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

60 citing papers in PubMed, 85 citations in OpenAlex.

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  7. [Association of metabolic syndrome and its components with gout: an analysis based on a large-scale health survey database].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Kelvin Ka-Lok WuDepartment of Health Technology and Informatics, The Hong Kong Polytechnic University, Hong Kong, China.
Samson Wing-Ming CheungDepartment of Health Technology and Informatics, The Hong Kong Polytechnic University, Hong Kong, China.
Kenneth King-Yip ChengDepartment of Health Technology and Informatics, The Hong Kong Polytechnic University, Hong Kong, China.ORCID 0000-0002-7274-0839
Hong Kong Polytechnic University · HK

Funding

National Natural Science Foundation of China 91857119PolyU internal funding Internal funding to Kenneth King Yip ChengResearch Grants Council, University Grants Committee 17100717Research Grants Council, University Grants Committee 17101815
6 · The paper itself

Abstract

Adipose tissue is an active endocrine and immune organ that controls systemic immunometabolism via multiple pathways. Diverse immune cell populations reside in adipose tissue, and their composition and immune responses vary with nutritional and environmental conditions. Adipose tissue dysfunction, characterized by sterile low-grade chronic inflammation and excessive immune cell infiltration, is a hallmark of obesity, as well as an important link to cardiometabolic diseases. Amongst the pro-inflammatory factors secreted by the dysfunctional adipose tissue, interleukin (IL)-1β, induced by the NLR family pyrin domain-containing 3 (NLRP3) inflammasome, not only impairs peripheral insulin sensitivity, but it also interferes with the endocrine and immune functions of adipose tissue in a paracrine manner. Human studies indicated that NLRP3 activity in adipose tissues positively correlates with obesity and its metabolic complications, and treatment with the IL-1β antibody improves glycaemia control in type 2 diabetic patients. In mouse models, genetic or pharmacological inhibition of NLRP3 activation pathways or IL-1β prevents adipose tissue dysfunction, including inflammation, fibrosis, defective lipid handling and adipogenesis, which in turn alleviates obesity and its related metabolic disorders. In this review, we summarize both the negative and positive regulators of NLRP3 inflammasome activation, and its pathophysiological consequences on immunometabolism. We also discuss the potential therapeutic approaches to targeting adipose tissue inflammasome for the treatment of obesity and its related metabolic disorders.

Indexed as

AdipokinesAdipose TissueAnimalsAutophagyDiabetes Mellitus, Type 2HumansInflammasomesInsulin ResistanceLipid MetabolismLipopolysaccharidesMetabolic DiseasesMiceNLR Family, Pyrin Domain-Containing 3 ProteinObesityPanniculitisAdipokinesInflammasomesLipopolysaccharidesNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanadipose tissueIL-1βimmunometabolisminsulin sensitivitymetabolic diseaseNLRP3 inflammasomeobesity

Identifiers

PMID32545355
PMCPMC7312293
OpenAlexW3034334444

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.