Evidence map›Paper›PMID 27048821›Full record

ReviewCellular and molecular life sciences : CMLS2016

Inflammasomes as polyvalent cell death platforms.

Nathalia M de Vasconcelos, Nina Van Opdenbosch, Mohamed Lamkanfi

Open access · bronzeAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
5.7field-weighted citation impact, top 4% 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

30 citing papers in PubMed, 59 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. NLRP3 inflammasome: The rising star in cardiovascular diseases.Frontiers in cardiovascular medicine · 2022
    Review
  6. Article
  7. Review
  8. Article
  9. The role of regulated necrosis in endocrine diseases.Nature reviews. Endocrinology · 2021
    Review
  10. Review
  11. Article
  12. Inflammasome-more Injury in Cholestasis.Cellular and molecular gastroenterology and hepatology · 2020
    Article
  13. Article
  14. Association ofGenes · 2019
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Review
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 2 institutions in 1 country.

Nathalia M de VasconcelosNOD-like Receptor and Inflammasome Laboratory, Inflammation Research Center, VIB, Technologiepark 927, B-9052, Zwijnaarde, Belgium.
Nina Van OpdenboschNOD-like Receptor and Inflammasome Laboratory, Inflammation Research Center, VIB, Technologiepark 927, B-9052, Zwijnaarde, Belgium.
Mohamed LamkanfiNOD-like Receptor and Inflammasome Laboratory, Inflammation Research Center, VIB, Technologiepark 927, B-9052, Zwijnaarde, Belgium. mohamed.lamkanfi@irc.vib-ugent.be.
VIB-UGent Center for Inflammation Research · BEGhent University · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammasomes are multi-protein platforms that are organized in the cytosol to cope with pathogens and cellular stress. The pattern recognition receptors NLRP1, NLRP3, NLRC4, AIM2 and Pyrin all assemble canonical platforms for caspase-1 activation, while caspase-11-dependent inflammasomes respond to intracellular Gram-negative pathogens. Inflammasomes are chiefly known for their roles in maturation and secretion of the inflammatory cytokines interleukin-(IL)1β and IL18, but they can also induce regulated cell death. Activation of caspases 1 and 11 in myeloid cells can trigger pyroptosis, a lytic and inflammatory cell death mode. Pyroptosis has been implicated in secretion of IL1β, IL18 and intracellular alarmins. Akin to these factors, it may have beneficial roles in controlling pathogen replication, but become detrimental in the context of chronic autoinflammatory diseases. Inflammasomes are increasingly implicated in induction of additional regulated cell death modes such as pyronecrosis and apoptosis. In this review, we overview recent advances in inflammasome-associated cell death research, illustrating the polyvalent roles of these macromolecular platforms in regulated cell death signaling.

Indexed as

AlarminsAnimalsApoptosisCaspase 1CaspasesCaspases, InitiatorGram-Negative BacteriaHumansInflammasomesInflammationInterleukin-18Interleukin-1betaMiceMice, KnockoutPyroptosisSignal TransductionAlarminsCasp4 protein, mouseCaspase 1CaspasesCaspases, InitiatorIL1B protein, mouseInflammasomesInterleukin-18Interleukin-1betaApoptosisCaspase-1Caspase-11Cell deathInflammasomeInflammationPyroptosis

Identifiers

PMID27048821
PMCPMC11108487
OpenAlexW2315306052

What OpenQuestion holds

Textmetadata
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.