Evidence map›Paper›PMID 28826530›Full record

ReviewAdvances in immunology2017

A Mechanistic Understanding of Pyroptosis: The Fiery Death Triggered by Invasive Infection.

Xing Liu, Judy Lieberman

Open access · greenAbstract readReview
In one paragraph

Review in Advances in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.

0numbers the graph read from it
0cells of the map it votes in
98citing papers in PubMed
25.3field-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

98 citing papers in PubMed, 170 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Mitochondrial DNA in Exercise-Mediated Innate Immune Responses.International journal of molecular sciences · 2025
    Review
  5. Article
  6. Supramolecular prodrug inspiried by theJournal of pharmaceutical analysis · 2025
    Article
  7. Article
  8. Review
  9. Review
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  13. Can We Exploit Inflammasomes for Host-Directed Therapy in the Fight againstInternational journal of molecular sciences · 2024
    Review
  14. Palmitoylation at a conserved cysteine residue facilitates gasdermin D-mediated pyroptosis and cytokine release.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

38 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 2 institutions in 1 country.

Xing LiuProgram in Cellular and Molecular Medicine, Boston Children's Hospital, Harvard Medical School, Boston, MA, United States.
Judy LiebermanProgram in Cellular and Molecular Medicine, Boston Children's Hospital, Harvard Medical School, Boston, MA, United States. Electronic address: judy.lieberman@childrens.harvard.edu.
Boston Children's Hospital · USHarvard University · US

Funding

Gasdermin E and pyroptosis in cancerR01CA240955 · NCI · BOSTON CHILDREN'S HOSPITAL · PI LIEBERMAN, JUDY · 2020 to 2024
$2.5M
NCI NIH HHS R01 CA240955
6 · The paper itself

Abstract

Immune cells and skin and mucosal epithelial cells recognize invasive microbes and other signs of danger to sound alarms that recruit responder cells and initiate an immediate "innate" immune response. An especially powerful alarm is triggered by cytosolic sensors of invasive infection that assemble into multimolecular complexes, called inflammasomes, that activate the inflammatory caspases, leading to maturation and secretion of proinflammatory cytokines and pyroptosis, an inflammatory death of the infected cell. Work in the past year has defined the molecular basis of pyroptosis. Activated inflammatory caspases cleave Gasdermin D (GSDMD), a cytosolic protein in immune antigen-presenting cells and epithelia. Cleavage separates the autoinhibitory C-terminal fragment from the active N-terminal fragment, which moves to the cell membrane, binds to lipids on the inside of the cell membrane, and oligomerizes to form membrane pores that disrupt cell membrane integrity, causing death and leakage of small molecules, including the proinflammatory cytokines and GSDMD itself. GSDMD also binds to cardiolipin on bacterial membranes and kills the very bacteria that activate the inflammasome. GSDMD belongs to a family of poorly studied gasdermins, expressed in the skin and mucosa, which can also form membrane pores. Spontaneous mutations that disrupt the binding of the N- and C-terminal domains of other gasdermins are associated with alopecia and asthma. Here, we review recent studies that identified the roles of the inflammasome, inflammatory caspases, and GSDMD in pyroptosis and highlight some of the outstanding questions about their roles in innate immunity, control of infection, and sepsis.

Indexed as

AnimalsAntigen-Presenting CellsBacterial InfectionsCaspasesCell MembraneCytokinesGasderminsGene Expression RegulationHIV InfectionsHumansImmunity, InnateInflammasomesIntracellular Signaling Peptides and ProteinsNeoplasm ProteinsPhosphate-Binding ProteinsProtein IsoformsCaspasesCytokinesGasderminsGSDMD protein, humanInflammasomesIntracellular Signaling Peptides and ProteinsNeoplasm ProteinsPhosphate-Binding ProteinsProtein IsoformsGasderminInflammasomeInflammatory caspasesPore-forming proteinPyroptosisSepsis

Identifiers

PMID28826530
PMCPMC10245508
OpenAlexW2598820457

What OpenQuestion holds

Textmetadata
LicenceTDM
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.