Evidence map›Paper›PMID 32641743›Full record

ReviewNature reviews. Rheumatology2020

Cell death in chronic inflammation: breaking the cycle to treat rheumatic disease.

Holly Anderton, Ian P Wicks, John Silke

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Rheumatology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed, 2 pooled it
6.5field-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

81 citing papers in PubMed, 2 syntheses or guidelines pooled it, 139 citations in OpenAlex.

  1. Pooled it
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  15. A viral necrosome mediates direct RIPK3 activation to promote inflammatory necroptosis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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  19. The dual role of PGAM5 in inflammation.Experimental & molecular medicine · 2025
    Review
  20. Cytokines in cancer.Cancer cell · 2025
    Review

21 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

3 authors at 2 institutions in 1 country.

Holly AndertonThe Walter and Eliza Hall Institute for Medical Research, Parkville, Melbourne, Victoria, Australia.ORCID http://orcid.org/0000-0003-3913-9686
Ian P WicksThe Walter and Eliza Hall Institute for Medical Research, Parkville, Melbourne, Victoria, Australia.
John SilkeThe Walter and Eliza Hall Institute for Medical Research, Parkville, Melbourne, Victoria, Australia. silke@wehi.edu.au.ORCID http://orcid.org/0000-0002-7611-5774
The University of Melbourne · AUThe Royal Melbourne Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cell death is a vital process that occurs in billions of cells in the human body every day. This process helps maintain tissue homeostasis, supports recovery from acute injury, deals with infection and regulates immunity. Cell death can also provoke inflammatory responses, and lytic forms of cell death can incite inflammation. Loss of cell membrane integrity leads to the uncontrolled release of damage-associated molecular patterns (DAMPs), which are normally sequestered inside cells. Such DAMPs increase local inflammation and promote the production of cytokines and chemokines that modulate the innate immune response. Cell death can be both a consequence and a cause of inflammation, which can be difficult to distinguish in chronic diseases. Despite this caveat, excessive or poorly regulated cell death is increasingly recognized as a contributor to chronic inflammation in rheumatic disease and other inflammatory conditions. Drugs that inhibit cell death could, therefore, be used therapeutically for the treatment of these diseases, and programmes to develop such inhibitors are already underway. In this Review, we outline pathways for the major cell death programmes (apoptosis, necroptosis, pyroptosis and NETosis) and their potential roles in chronic inflammation. We also discuss current and developing therapies that target the cell death machinery.

Indexed as

AlarminsAnimalsAntibodies, Monoclonal, HumanizedApoptosisCell DeathChemokinesChronic DiseaseCytokinesExtracellular TrapsHomeostasisHumansImmunity, InnateImmunologic FactorsInflammationMiceModels, AnimalAlarminsAntibodies, Monoclonal, HumanizedChemokinesCytokinesImmunologic Factors

Identifiers

PMID32641743
OpenAlexW3040804126

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.