Evidence map›Paper›PMID 25493335›Full record

ReviewAnnual review of immunology2015

Programmed necrosis in the cross talk of cell death and inflammation.

Francis Ka-Ming Chan, Nivea Farias Luz, Kenta Moriwaki

Open access · greenAbstract readReview
In one paragraph

Review in Annual review of immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 215 papers.

0numbers the graph read from it
0cells of the map it votes in
215citing papers in PubMed
12.0field-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

215 citing papers in PubMed, 355 citations in OpenAlex.

  1. Review
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  9. mBio · 2025
    Article
  10. Article
  11. Review
  12. PARP12-mediated mono-ADP-ribosylation as a checkpoint for necroptosis and apoptosis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Necroptosis in obesity: a complex cell death event.Apoptosis : an international journal on programmed cell death · 2025
    Review
  18. Article
  19. Article
  20. Article

155 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 2 countries.

Francis Ka-Ming ChanDepartment of Pathology, Immunology and Microbiology Program, University of Massachusetts Medical School, Worcester, Massachusetts 01605; email: Francis.chan@umassmed.edu.
Nivea Farias Luz
Kenta Moriwaki
University of Massachusetts Chan Medical School · US

Funding

Programmed necrosis in Immune ResponsesR01AI083497 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CHAN, FRANCIS KAMING · 2010 to 2013
$1.6M
NIAID NIH HHS AI083497NIAID NIH HHS R01 AI083497
6 · The paper itself

Abstract

Cell proliferation and cell death are integral elements in maintaining homeostatic balance in metazoans. Disease pathologies ensue when these processes are disturbed. A plethora of evidence indicates that malfunction of cell death can lead to inflammation, autoimmunity, or immunodeficiency. Programmed necrosis or necroptosis is a form of nonapoptotic cell death driven by the receptor interacting protein kinase 3 (RIPK3) and its substrate, mixed lineage kinase domain-like (MLKL). RIPK3 partners with its upstream adaptors RIPK1, TRIF, or DAI to signal for necroptosis in response to death receptor or Toll-like receptor stimulation, pathogen infection, or sterile cell injury. Necroptosis promotes inflammation through leakage of cellular contents from damaged plasma membranes. Intriguingly, many of the signal adaptors of necroptosis have dual functions in innate immune signaling. This unique signature illustrates the cooperative nature of necroptosis and innate inflammatory signaling pathways in managing cell and organismal stresses from pathogen infection and sterile tissue injury.

Indexed as

Signal TransductionAnimalsBacterial InfectionsBiological EvolutionCell DeathHumansInflammasomesInflammationInterleukin-1betaNecrosisNF-kappa BParasitic DiseasesPhosphorylationProtein BindingReceptor-Interacting Protein Serine-Threonine KinasesUbiquitinationInflammasomesInterleukin-1betaNF-kappa BReceptor-Interacting Protein Serine-Threonine KinasesDAIinflammationMCMVMLKLnecroptosisRIPK1RIPK3TNFTRIFvaccinia virus

Identifiers

PMID25493335
PMCPMC4394030
OpenAlexW2159679709

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.