Evidence map›Paper›PMID 41876821›Full record

ReviewExperimental & molecular medicine2026

Molecular mechanisms of NLRP3 inflammasome activation.

Hyo Jung Shin, In Soo Kim, Jin Kyung Kim, Eun-Kyeong Jo

Abstract readReview
In one paragraph

Review in Experimental & molecular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

18 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  3. Modulation of the gut microbiota by traditional Chinese medicine to attenuate chemotherapy-induced toxicity in gastric cancer: a review.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 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

4 authors.

Hyo Jung ShinDepartment of Biochemistry and Cell Biology, Eulji University School of Medicine, Daejeon, Republic of Korea.
In Soo KimDepartment of Medical Science, Chungnam National University College of Medicine, Daejeon, Republic of Korea.
Jin Kyung KimDepartment of Microbiology, Keimyung University School of Medicine, Daegu, Republic of Korea.ORCID http://orcid.org/0000-0002-2051-5787
Eun-Kyeong JoDepartment of Medical Science, Chungnam National University College of Medicine, Daejeon, Republic of Korea. hayoungj@cnu.ac.kr.ORCID http://orcid.org/0000-0001-7191-0587

Funding

National Research Foundation of Korea (NRF) RS-2021-NR061880National Research Foundation of Korea (NRF) RS-2023-00255021National Research Foundation of Korea (NRF) RS-2023-00277498
6 · The paper itself

Abstract

The NOD-like receptor protein 3 (NLRP3) inflammasome is among the most extensively studied multiprotein complexes, driving the maturation of pro-interleukin-1β (pro-IL-1β) and pro-IL-18-into their active forms, IL-1β and IL-18, respectively. The activation of the NLRP3 inflammasome is a multifaceted process triggered by a diverse array of stimuli, including pathogens, environmental particles and endogenous stress signals. Previously, NLRP3 inflammasome activation was considered a straightforward two-step process: signal 1, which induces the expression of NLRP3 and proinflammatory cytokines, and signal 2, which promotes the assembly of the inflammasome complex through mechanisms such as ionic fluxes, mitochondrial dysfunction and lysosomal damage. However, more intricate mechanisms have now been elucidated, particularly regarding the 'priming' step, involving the regulation of its post-translational modifications. Recent studies have comprehensively identified the core components of the NLRP3 inflammasome complex, its interacting complex partners, and regulatory mechanisms. Here we delve into the current understanding of the NLRP3 inflammasome activation mechanisms and explore its regulatory networks. Enhanced insights into the molecular and signaling pathways controlling this specialized inflammasome activation may pave the way for novel applications of NLRP3 inflammasome regulation to advance human health and prevent numerous diseases linked to the NLRP3 inflammasome.

Indexed as

InflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinAnimalsHumansSignal TransductionInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, human

Identifiers

PMID41876821
PMCPMC13049041

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Registered trials

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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.