Evidence map›Paper›PMID 29593066›Full record

ReviewGenes & development2018

Necroptosis in development and diseases.

Bing Shan, Heling Pan, Ayaz Najafov, Junying Yuan

Open access · diamondAbstract readReview
In one paragraph

Review in Genes & development, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 221 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
221citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

221 citing papers in PubMed, 1 synthesis or guideline pooled it, 346 citations in OpenAlex.

  1. Pooled it
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  3. Review
  4. Review
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  7. Article
  8. Article
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  11. Review
  12. Host Responses to SARS-CoV-2 with an Emphasis on Cytokines.International journal of molecular sciences · 2026
    Review
  13. Review
  14. Article
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  16. Review
  17. Review
  18. Article
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  20. bioRxiv : the preprint server for biology · 2025
    Article

161 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 2 institutions in 2 countries.

Bing Shan *Interdisciplinary Research Center on Biology and Chemistry, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, PuDong District, Shanghai 201203, China.
Heling Pan *Interdisciplinary Research Center on Biology and Chemistry, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, PuDong District, Shanghai 201203, China.
Ayaz NajafovDepartment of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA.
Junying YuanInterdisciplinary Research Center on Biology and Chemistry, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, PuDong District, Shanghai 201203, China.
Chinese Academy of Sciences · CNHarvard University · US

Funding

Single cell RNA-seq analyses of age-related changes in glial cells and in ADRF1AG055521 · NIA · HARVARD MEDICAL SCHOOL · PI YUAN, JUNYING · 2017 to 2017
$2.9M
Investigating the neuroinflammatory role of RIP1 kinaseR01AG047231 · NIA · HARVARD MEDICAL SCHOOL · PI YUAN, JUNYING · 2014 to 2018
$2.2M
Investigating the mechanism of TNFalpha mediated cell death in oligodendrocytesR01NS082257 · NINDS · HARVARD MEDICAL SCHOOL · PI YUAN, JUNYING · 2013 to 2017
$1.9M
NIA NIH HHS R01 AG047231NIA NIH HHS RF1 AG055521NINDS NIH HHS R01 NS082257
6 · The paper itself

Abstract

Necroptosis, a form of regulated necrotic cell death mediated by RIPK1 (receptor-interacting protein kinase 1) kinase activity, RIPK3, and MLKL (mixed-lineage kinase domain-like pseudokinase), can be activated under apoptosis-deficient conditions. Modulating the activation of RIPK1 by ubiquitination and phosphorylation is critical to control both necroptosis and apoptosis. Mutant mice with kinase-dead RIPK1 or RIPK3 and MLKL deficiency show no detrimental phenotype in regard to development and adult homeostasis. However, necroptosis and apoptosis can be activated in response to various mutations that result in the abortion of the defective embryos and human inflammatory and neurodegenerative pathologies. RIPK1 inhibition represents a key therapeutic strategy for treatment of diseases where blocking both necroptosis and apoptosis can be beneficial.

Indexed as

DiseaseApoptosisCell DeathGrowth and DevelopmentMutationNuclear ProteinsReceptor-Interacting Protein Serine-Threonine KinasesSignal TransductionTumor Necrosis Factor-alphaNuclear ProteinsReceptor-Interacting Protein Serine-Threonine KinasesTumor Necrosis Factor-alphaapoptosisMLKLnecroptosisRIPK1RIPK3

Identifiers

PMID29593066
PMCPMC5900707
OpenAlexW2795155279

What OpenQuestion holds

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LicenceCC BY-NC
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.