Evidence map›Paper›PMID 32883606›Full record

ReviewCytokine & growth factor reviews2020

Mechanisms of NLRP3 priming in inflammaging and age related diseases.

Anna Gritsenko, Jack P Green, David Brough, Gloria Lopez-Castejon

Open access · hybridAbstract readReview
In one paragraph

Review in Cytokine & growth factor reviews, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

83 citing papers in PubMed, 120 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Therapeutic Potential of 1‑(1,2,3,5,6,7-Hexahydro‑ACS pharmacology & translational science · 2026
    Article
  7. Immune Aging as a Failure of Programmed Cell Death Coordination.International journal of molecular sciences · 2026
    Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Potential Role of Inflammasomes in Aging.International journal of molecular sciences · 2025
    Review
  16. Review
  17. Review
  18. Article
  19. Cardio-Rheumatic Diseases: Inflammasomes Behaving Badly.International journal of molecular sciences · 2025
    Review
  20. Article

23 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

4 authors at 1 institution in 1 country.

Anna GritsenkoLydia Becker Institute of Immunology and Inflammation, Division of Infection, Immunity and Respiratory Medicine, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK.
Jack P GreenLydia Becker Institute of Immunology and Inflammation, Division of Neuroscience and Experimental Psychology, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK.
David BroughLydia Becker Institute of Immunology and Inflammation, Division of Neuroscience and Experimental Psychology, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK.
Gloria Lopez-CastejonLydia Becker Institute of Immunology and Inflammation, Division of Infection, Immunity and Respiratory Medicine, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK. Electronic address: Gloria.lopez-castejon@manchester.ac.uk.
Manchester Academic Health Science Centre · GB

Funding

Medical Research Council MR/N013751/1Medical Research Council MR/N029992/1Medical Research Council MR/T016515/1Wellcome Trust 104192/Z/14/Z
6 · The paper itself

Abstract

The NLRP3 inflammasome is a vital part of the innate immune response, whilst its aberrant activation drives the progression of a number of non-communicable diseases. Thus, NLRP3 inflammasome assembly must be tightly controlled at several checkpoints. The priming step of NLRP3 inflammasome activation is associated with increased NLRP3 gene expression, as well as post-translational modifications that control NLRP3 levels and licence the NLRP3 protein for inflammasome assembly. Increasing life expectancy in modern society is accompanied by a growing percentage of elderly individuals. The process of aging is associated with chronic inflammation that drives and/or worsens a range of age related non-communicable conditions. The NLRP3 inflammasome is known to contribute to pathological inflammation in many settings, but the mechanisms that prime NLRP3 for activation throughout aging and related co-morbidities have not been extensively reviewed. Here we dissect the biochemical changes that occur during aging and the pathogenesis of age related diseases and analyse the mechanisms by which they prime the NLRP3 inflammasome, thus exacerbating inflammation.

Indexed as

InflammasomesInflammationNLR Family, Pyrin Domain-Containing 3 ProteinAgedAge FactorsHumansImmunity, InnateInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanAgingInflammagingInflammasomeNLRP3PrimingSenescence

Identifiers

PMID32883606
PMCPMC7571497
OpenAlexW3081231483

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.