Evidence map›Paper›PMID 35563804›Full record

ReviewCells2022

It's All in the PAN: Crosstalk, Plasticity, Redundancies, Switches, and Interconnectedness Encompassed by PANoptosis Underlying the Totality of Cell Death-Associated Biological Effects.

Jessica M Gullett, Rebecca E Tweedell, Thirumala-Devi Kanneganti

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
8.0field-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

77 citing papers in PubMed, 100 citations in OpenAlex.

  1. Article
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  14. Review
  15. Research progress in PANoptosis mechanisms and their interplay with tuberculosis.Frontiers in cellular and infection microbiology · 2026
    Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

17 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 1 institution in 1 country.

Jessica M GullettDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.ORCID 0000-0003-3996-9110
Rebecca E TweedellDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.ORCID 0000-0003-3442-9609
Thirumala-Devi KannegantiDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.ORCID 0000-0002-6395-6443
St. Jude Children's Research Hospital · US

Funding

Innate immune sensors, inflammasomes, and inflammasome-mediated processes in cancerR35CA253095 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI Thirumala-Devi Kanneganti · 2020 to 2026
$7.0M
Role of NLR Inflammasomes in Autoinflammatory Diseases and Host DefenseR01AR056296 · NIAMS · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI KANNEGANTI, THIRUMALA-DEVI · 2008 to 2022
$5.9M
The Non-Inflammasome NLRs in Immunity and Host defenseR01AI124346 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI Thirumala-Devi Kanneganti · 2016 to 2026
$5.8M
Inflammatory Caspases in Innate Immunity and InflammationR37AI101935 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI Thirumala-Devi Kanneganti · 2017 to 2026
$4.9M
Targeting innate immune pathways, and inflammatory cell death in cytokine-mediated diseasesR01AI160179 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI KANNEGANTI, THIRUMALA-DEVI · 2021 to 2025
$4.2M
Inflammatory Caspases in Innate Immunity and InflammationR01AI101935 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI KANNEGANTI, THIRUMALA-DEVI · 2012 to 2016
$2.2M
NCI NIH HHS R35 CA253095NIAID NIH HHS R01 AI101935NIAID NIH HHS R01 AI124346NIAID NIH HHS R01 AI160179NIAID NIH HHS R37 AI101935NIAMS NIH HHS R01 AR056296
6 · The paper itself

Abstract

The innate immune system provides the first line of defense against cellular perturbations. Innate immune activation elicits inflammatory programmed cell death in response to microbial infections or alterations in cellular homeostasis. Among the most well-characterized programmed cell death pathways are pyroptosis, apoptosis, and necroptosis. While these pathways have historically been defined as segregated and independent processes, mounting evidence shows significant crosstalk among them. These molecular interactions have been described as 'crosstalk', 'plasticity', 'redundancies', 'molecular switches', and more. Here, we discuss the key components of cell death pathways and note several examples of crosstalk. We then explain how the diverse descriptions of crosstalk throughout the literature can be interpreted through the lens of an integrated inflammatory cell death concept, PANoptosis. The totality of biological effects in PANoptosis cannot be individually accounted for by pyroptosis, apoptosis, or necroptosis alone. We also discuss PANoptosomes, which are multifaceted macromolecular complexes that regulate PANoptosis. We consider the evidence for PANoptosis, which has been mechanistically characterized during influenza A virus, herpes simplex virus 1,

Indexed as

Herpesvirus 1, HumanNecroptosisApoptosisCell DeathPyroptosisAIM2apoptosisASCcaspasecaspase-1caspase-3caspase-7caspase-8crosstalkinfectioninflammasomeinflammationinflammatory cell deathinnate immunityIRF1MLKLnecroptosisNLRNLRP3PANoptosisPANoptosomeplasticityPyrinpyroptosisredundancyRIPK1RIPK3ZBP1

Identifiers

PMID35563804
PMCPMC9105755
OpenAlexW4225137984

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.