Evidence map›Paper›PMID 32152420›Full record

ReviewCell research2020

Toward targeting inflammasomes: insights into their regulation and activation.

Shelbi Christgen, David E Place, Thirumala-Devi Kanneganti

Open access · hybridAbstract readReview
In one paragraph

Review in Cell research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 160 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
160citing papers in PubMed, 2 pooled it
15.1field-weighted citation impact, top 1% 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

160 citing papers in PubMed, 2 syntheses or guidelines pooled it, 280 citations in OpenAlex.

  1. Pooled it
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  7. Interleukin-18 Inhibition Aggravates Atherosclerosis in Jak2JACC. Basic to translational science · 2026
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  19. R-loops: a key driver of inflammatory responses in cancer.Experimental & molecular medicine · 2025
    Review
  20. Review

100 more citing papers are in PubMed but not listed here.

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.

Shelbi ChristgenDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN, 38105, USA.
David E PlaceDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN, 38105, USA.
Thirumala-Devi KannegantiDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN, 38105, USA. thirumala-devi.kanneganti@stjude.org.ORCID http://orcid.org/0000-0002-6395-6443
St. Jude Children's Research Hospital · US

Funding

Role of NLR Inflammasomes in Autoinflammatory Diseases and Host DefenseR01AR056296 · NIAMS · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI KANNEGANTI, THIRUMALA-DEVI · 2008 to 2022
$5.9M
The Non-Inflammasome NLRs in Immunity and Host defenseR01AI124346 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI Thirumala-Devi Kanneganti · 2016 to 2026
$5.8M
Inflammatory Caspases in Innate Immunity and InflammationR37AI101935 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI Thirumala-Devi Kanneganti · 2017 to 2026
$4.9M
NLR signaling in colitis and colorectal tumorigenesisR01CA163507 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI KANNEGANTI, THIRUMALA-DEVI · 2012 to 2020
$3.5M
Inflammatory Caspases in Innate Immunity and InflammationR01AI101935 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI KANNEGANTI, THIRUMALA-DEVI · 2012 to 2016
$2.2M
NCI NIH HHS R01 CA163507NIAID NIH HHS R01 AI101935NIAID NIH HHS R01 AI124346NIAID NIH HHS R37 AI101935NIAMS NIH HHS R01 AR056296
6 · The paper itself

Abstract

Inflammasomes are multi-component signaling complexes critical to the initiation of pyroptotic cell death in response to invading pathogens and cellular damage. A number of innate immune receptors have been reported to serve as inflammasome sensors. Activation of these sensors leads to the proteolytic activation of caspase-1, a proinflammatory caspase responsible for the cleavage of proinflammatory cytokines interleukin-1β and interleukin-18 and the effector of pyroptotic cell death, gasdermin D. Though crucial to the innate immune response to infection, dysregulation of inflammasome activation can lead to the development of inflammatory diseases, neurodegeneration, and cancer. Therefore, clinical interest in the modulation of inflammasome activation is swiftly growing. As such, it is imperative to develop a mechanistic understanding of the regulation of these complexes. In this review, we divide the regulation of inflammasome activation into three parts. We discuss the transcriptional regulation of inflammasome components and related proteins, the post-translational mechanisms of inflammasome activation, and advances in the understanding of the structural basis of inflammasome activation.

Indexed as

AnimalsCaspase 1GasderminsGene Expression RegulationHumansImmunity, InnateInflammasomesInterleukin-18Interleukin-1betaIntracellular Signaling Peptides and ProteinsPhosphate-Binding ProteinsPyroptosisSignal TransductionCaspase 1GasderminsGSDMD protein, humanIL18 protein, humanInflammasomesInterleukin-18Interleukin-1betaIntracellular Signaling Peptides and ProteinsPhosphate-Binding Proteins

Identifiers

PMID32152420
PMCPMC7118104
OpenAlexW3009886233

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.