Evidence map›Paper›PMID 33603747›Full record

ReviewFrontiers in immunology2020

Regulation of the NLRP3 Inflammasome by Post-Translational Modifications and Small Molecules.

Jin Kyung Seok, Han Chang Kang, Yong-Yeon Cho, Hye Suk Lee, Joo Young Lee

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
5.4field-weighted citation impact, top 3% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.

  1. Pooled it
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  12. A full-spectrumFrontiers in pharmacology · 2025
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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

5 authors at 1 institution in 1 country.

Jin Kyung SeokBK21 PLUS Team, College of Pharmacy, The Catholic University of Korea, Bucheon, South Korea.
Han Chang KangBK21 PLUS Team, College of Pharmacy, The Catholic University of Korea, Bucheon, South Korea.
Yong-Yeon ChoBK21 PLUS Team, College of Pharmacy, The Catholic University of Korea, Bucheon, South Korea.
Hye Suk LeeBK21 PLUS Team, College of Pharmacy, The Catholic University of Korea, Bucheon, South Korea.
Joo Young LeeBK21 PLUS Team, College of Pharmacy, The Catholic University of Korea, Bucheon, South Korea.
Catholic University of Korea · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammation is a host protection mechanism that eliminates invasive pathogens from the body. However, chronic inflammation, which occurs repeatedly and continuously over a long period, can directly damage tissues and cause various inflammatory and autoimmune diseases. Pattern recognition receptors (PRRs) respond to exogenous infectious agents called pathogen-associated molecular patterns and endogenous danger signals called danger-associated molecular patterns. Among PRRs, recent advancements in studies of the NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome have established its significant contribution to the pathology of various inflammatory diseases, including metabolic disorders, immune diseases, cardiovascular diseases, and cancer. The regulation of NLRP3 activation is now considered to be important for the development of potential therapeutic strategies. To this end, there is a need to elucidate the regulatory mechanism of NLRP3 inflammasome activation by multiple signaling pathways, post-translational modifications, and cellular organelles. In this review, we discuss the intracellular signaling events, post-translational modifications, small molecules, and phytochemicals participating in the regulation of NLRP3 inflammasome activation. Understanding how intracellular events and small molecule inhibitors regulate NLRP3 inflammasome activation will provide crucial information for elucidating the associated host defense mechanism and the development of efficient therapeutic strategies for chronic diseases.

Indexed as

AnimalsHumansInflammasomesInflammationNLR Family, Pyrin Domain-Containing 3 ProteinProtein Processing, Post-TranslationalSignal TransductionInflammasomesNLR Family, Pyrin Domain-Containing 3 Proteincell signalinginflammationinnate immunitypattern-recognition receptorspharmacological inhibitor

Identifiers

PMID33603747
PMCPMC7884467
OpenAlexW3128374923

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.