Evidence map›Paper›PMID 31064994›Full record

ArticleNature communications2019

Caspase-1 initiates apoptosis in the absence of gasdermin D.

Kohsuke Tsuchiya, Shinsuke Nakajima, Shoko Hosojima, Dinh Thi Nguyen, Tsuyoshi Hattori, Thuong Manh Le, Osamu Hori, Mamunur Rashid Mahib, Yoshifumi Yamaguchi, Masayuki Miura and 5 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 304 papers.

0numbers the graph read from it
0cells of the map it votes in
304citing papers in PubMed
21.4field-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

304 citing papers in PubMed, 481 citations in OpenAlex.

  1. Trial
  2. Trial
  3. The gasdermin family: from pyroptosis mechanisms to therapeutic targets.Signal transduction and targeted therapy · 2026
    Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. How to recognize if a cell dies from pyroptosis?Molecular biology reports · 2026
    Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

244 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

15 authors at 4 institutions in 1 country.

Kohsuke TsuchiyaDivision of Immunology and Molecular Biology, Cancer Research Institute, Kanazawa University, Kakuma-machi, Kanazawa, 920-1192, Japan. ktsuchiya@staff.kanazawa-u.ac.jp.
Shinsuke NakajimaDivision of Immunology and Molecular Biology, Cancer Research Institute, Kanazawa University, Kakuma-machi, Kanazawa, 920-1192, Japan.
Shoko HosojimaDivision of Immunology and Molecular Biology, Cancer Research Institute, Kanazawa University, Kakuma-machi, Kanazawa, 920-1192, Japan.
Dinh Thi NguyenDepartment of Neuroanatomy, Graduate School of Medical Sciences, Kanazawa University, 13-1 Takara-Machi, Kanazawa, 920-8640, Japan.ORCID http://orcid.org/0000-0002-2910-0879
Tsuyoshi HattoriDepartment of Neuroanatomy, Graduate School of Medical Sciences, Kanazawa University, 13-1 Takara-Machi, Kanazawa, 920-8640, Japan.ORCID http://orcid.org/0000-0002-8168-8710
Thuong Manh LeDepartment of Neuroanatomy, Graduate School of Medical Sciences, Kanazawa University, 13-1 Takara-Machi, Kanazawa, 920-8640, Japan.
Osamu HoriDepartment of Neuroanatomy, Graduate School of Medical Sciences, Kanazawa University, 13-1 Takara-Machi, Kanazawa, 920-8640, Japan.
Mamunur Rashid MahibDivision of Immunology and Molecular Biology, Cancer Research Institute, Kanazawa University, Kakuma-machi, Kanazawa, 920-1192, Japan.
Yoshifumi YamaguchiInstitute of Low Temperature Science, Hokkaido University, Kita-19, Nishi-8, Kita-ku, Sapporo, 060-0819, Japan.ORCID http://orcid.org/0000-0001-7340-4557
Masayuki MiuraDepartment of Genetics, Graduate School of Pharmaceutical Sciences, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan.ORCID http://orcid.org/0000-0001-7444-5705
Takeshi KinoshitaDivision of Immunology and Molecular Biology, Cancer Research Institute, Kanazawa University, Kakuma-machi, Kanazawa, 920-1192, Japan.
Hiroko KushiyamaDivision of Immunology and Molecular Biology, Cancer Research Institute, Kanazawa University, Kakuma-machi, Kanazawa, 920-1192, Japan.
Mayumi SakuraiDivision of Immunology and Molecular Biology, Cancer Research Institute, Kanazawa University, Kakuma-machi, Kanazawa, 920-1192, Japan.
Toshihiko ShiroishiMammalian Genetics Laboratory, Genetic Strains Research Center, National Institute of Genetics, 1111 Yata, Mishima, Shizuoka, 411-8540, Japan.
Takashi SudaDivision of Immunology and Molecular Biology, Cancer Research Institute, Kanazawa University, Kakuma-machi, Kanazawa, 920-1192, Japan. sudat@staff.kanazawa-u.ac.jp.
Kanazawa University · JPHokkaido University · JPNational Institute of Genetics · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Caspase-1 activated in inflammasomes triggers a programmed necrosis called pyroptosis, which is mediated by gasdermin D (GSDMD). However, GSDMD-deficient cells are still susceptible to caspase-1-mediated cell death. Therefore, here, we investigate the mechanism of caspase-1-initiated cell death in GSDMD-deficient cells. Inflammasome stimuli induce apoptosis accompanied by caspase-3 activation in GSDMD-deficient macrophages, which largely relies on caspase-1. Chemical dimerization of caspase-1 induces pyroptosis in GSDMD-sufficient cells, but apoptosis in GSDMD-deficient cells. Caspase-1-induced apoptosis involves the Bid-caspase-9-caspase-3 axis, which can be followed by GSDME-dependent secondary necrosis/pyroptosis. However, Bid ablation does not completely abolish the cell death, suggesting the existence of an additional mechanism. Furthermore, cortical neurons and mast cells exhibit little or low GSDMD expression and undergo apoptosis after oxygen glucose deprivation and nigericin stimulation, respectively, in a caspase-1- and Bid-dependent manner. This study clarifies the molecular mechanism and biological roles of caspase-1-induced apoptosis in GSDMD-low/null cell types.

Indexed as

AnimalsApoptosis Regulatory ProteinsBH3 Interacting Domain Death Agonist ProteinCaspase 1Caspase 3Caspase 9Cell Line, TumorCerebral CortexEmbryo, MammalianGasderminsGene Knockout TechniquesInflammasomesIntracellular Signaling Peptides and ProteinsMacrophagesMiceMice, Inbred C57BLApoptosis Regulatory ProteinsBH3 Interacting Domain Death Agonist ProteinBid protein, mouseCasp1 protein, mouseCasp3 protein, mouseCasp9 protein, mouseCaspase 1Caspase 3Caspase 9GasderminsGsdmd protein, mouseGsdme protein, mouseInflammasomesIntracellular Signaling Peptides and ProteinsNigericinPhosphate-Binding ProteinsReceptors, Estrogen

Identifiers

PMID31064994
PMCPMC6505044
OpenAlexW2944565286

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.