Evidence map›Paper›PMID 28498367›Full record

ReviewCell death and differentiation2017

Initiation and execution mechanisms of necroptosis: an overview.

Sasker Grootjans, Tom Vanden Berghe, Peter Vandenabeele

Open access · bronzeAbstract readReview
In one paragraph

Review in Cell death and differentiation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 331 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
331citing papers in PubMed, 2 pooled it
17.9field-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

331 citing papers in PubMed, 2 syntheses or guidelines pooled it, 547 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Regulated Cell Death in Idiopathic Pulmonary Fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article

271 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.

Sasker GrootjansMolecular Signaling and Cell Death unit, VIB Inflammation Research Center, 9000 Ghent, Belgium.
Tom Vanden BergheMolecular Signaling and Cell Death unit, VIB Inflammation Research Center, 9000 Ghent, Belgium.
Peter VandenabeeleMolecular Signaling and Cell Death unit, VIB Inflammation Research Center, 9000 Ghent, Belgium.ORCID 0000-0002-6669-8822
Ghent University · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Necroptosis is a form of regulated cell death, which is induced by ligand binding to TNF family death domain receptors, pattern recognizing receptors and virus sensors. The common feature of these receptor systems is the implication of proteins, which contain a receptor interaction protein kinase (RIPK) homology interaction motif (RHIM) mediating recruitment and activation of receptor-interacting protein kinase 3 (RIPK3), which ultimately activates the necroptosis executioner mixed lineage kinase domain-like (MLKL). In case of the TNF family members, the initiator is the survival- and cell death-regulating RIPK1 kinase, in the case of Toll-like receptor 3/4 (TLR3/4), a RHIM-containing adaptor, called TRIF, while in the case of Z-DNA-binding protein ZBP1/DAI, the cytosolic viral sensor itself contains a RHIM domain. In this review, we discuss the different protein complexes that serve as nucleation platforms for necroptosis and the mechanism of execution of necroptosis. Transgenic models (knockout, kinase-dead knock-in) and pharmacologic inhibition indicate that RIPK1, RIPK3 or MLKL are implicated in many inflammatory, degenerative and infectious diseases. However, the conclusion of necroptosis being solely involved in the etiology of diseases is blurred by the pleiotropic roles of RIPK1 and RIPK3 in other cellular processes such as apoptosis and inflammasome activation.

Indexed as

ApoptosisAmyloidAnimalsHumansModels, BiologicalNecrosisReceptor-Interacting Protein Serine-Threonine KinasesSignal TransductionAmyloidReceptor-Interacting Protein Serine-Threonine Kinases

Identifiers

PMID28498367
PMCPMC5520172
OpenAlexW2612992363

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.