Evidence map›Paper›PMID 33852854›Full record

ArticleCell reports2021

Gasdermin E permits interleukin-1 beta release in distinct sublytic and pyroptotic phases.

Bowen Zhou, Derek W Abbott

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

89 citing papers in PubMed, 122 citations in OpenAlex.

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  14. Nature-inspired IL-1 targeted therapy to treat chronic inflammatory diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  15. Review
  16. Human non-canonical inflammasomes activate CASP3 to limit intracellularbioRxiv : the preprint server for biology · 2025
    Article
  17. Review
  18. Article
  19. Article
  20. Review

29 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

2 authors at 1 institution in 1 country.

Bowen ZhouDepartment of Pathology, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA.
Derek W AbbottDepartment of Pathology, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA. Electronic address: dwa4@case.edu.
University School · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007250 · NIGMS · CASE WESTERN RESERVE UNIVERSITY · PI HUANG, ALEX YEE-CHEN · 1985 to 2023
$33.4M
Molecular mechanisms of gasdermin recognition by proteases and autophagy proteins in cytokine releaseP01AI141350 · NIAID · CASE WESTERN RESERVE UNIVERSITY · PI DUBYAK, GEORGE R · 2020 to 2024
$9.4M
Innate Immune Signal Transduction Specificity in Inflammatory DiseaseR01GM086550 · NIGMS · CASE WESTERN RESERVE UNIVERSITY · PI ABBOTT, DEREK W · 2009 to 2020
$3.8M
Immunology Training Program-PredoctoralT32AI089474 · NIAID · CASE WESTERN RESERVE UNIVERSITY · PI COBB, BRIAN A · 2010 to 2025
$3.4M
Innate Immune Signal Transduction Specificity in Inflammatory DiseaseR35GM141603 · NIGMS · NATIONAL JEWISH HEALTH · PI Derek W Abbott · 2021 to 2026
$1.9M
NIAID NIH HHS P01 AI141350NIAID NIH HHS T32 AI089474NIGMS NIH HHS R01 GM086550NIGMS NIH HHS R35 GM141603NIGMS NIH HHS T32 GM007250
6 · The paper itself

Abstract

Cellular inflammasome activation causes caspase-1 cleavage of the pore-forming protein gasdermin D (GSDMD) with subsequent pyroptotic cell death and cytokine release. Here, we clarify the ambiguous role of the related family member gasdermin E (GSDME) in this process. Inflammasome stimulation in GSDMD-deficient cells led to apoptotic caspase cleavage of GSDME. Endogenous GSDME activation permitted sublytic, continuous interleukin-1β (IL-1β) release and membrane leakage, even in GSDMD-sufficient cells, whereas ectopic expression led to pyroptosis with GSDME oligomerization and complete liberation of IL-1β akin to GSDMD pyroptosis. We find that NLRP3 and NLRP1 inflammasomes ultimately rely concurrently on both gasdermins for IL-1β processing and release separately from their ability to induce cell lysis. Our study thus identifies GSDME as a conduit for IL-1β release independent of its ability to cause cell death.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsApoptosis Regulatory ProteinsCaspase 1Caspase 3Cell Line, TransformedGasderminsGene Expression RegulationGene Knockout TechniquesHumansInflammasomesInterleukin-1betaLipopolysaccharidesMacrophagesMiceNLR Family, Pyrin Domain-Containing 3 ProteinAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsCasp1 protein, mouseCasp3 protein, mouseCaspase 1Caspase 3GasderminsGsdmd protein, mouseGsdme protein, mouseIL1B protein, mouseInflammasomesInterleukin-1betaLipopolysaccharidesNALP1 protein, mouseNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mousePhosphate-Binding ProteinsPore Forming Cytotoxic Proteinscell deathgasdermin Dgasdermin EgasderminsGSDMDGSDMEIL-1inflammasomeinterleukin-1pore-forming proteins

Identifiers

PMID33852854
PMCPMC8106763
OpenAlexW3153860035

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.