Evidence map›Paper›PMID 27959630›Full record

ReviewAnnual review of pathology2017

Necroptosis: Mechanisms and Relevance to Disease.

Lorenzo Galluzzi, Oliver Kepp, Francis Ka-Ming Chan, Guido Kroemer

Abstract readReview
In one paragraph

Review in Annual review of pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 420 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
420citing 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

420 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Cuproptosis and the bioinorganic basis of copper-induced cell death.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2026
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360 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.

Lorenzo GalluzziDepartment of Radiation Oncology, Weill Cornell Medical College, New York, NY 10065; email: deadoc@vodafone.it.
Oliver KeppEquipe 11 labellisée Ligue contre le Cancer, Centre de Recherche des Cordeliers, 75006 Paris, France; email: kroemer@orange.fr.
Francis Ka-Ming ChanUniversity of Massachusetts Medical School, Worcester, Massachusetts 01065; email: francis.chan@umassmed.edu.
Guido KroemerEquipe 11 labellisée Ligue contre le Cancer, Centre de Recherche des Cordeliers, 75006 Paris, France; email: kroemer@orange.fr.

Funding

Necroptosis signaling adaptors in inflammatory diseasesR01AI119030 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CHAN, FRANCIS KAMING · 2016 to 2019
$1.6M
NIAID NIH HHS R01 AI119030
6 · The paper itself

Abstract

Necroptosis is a form of regulated cell death that critically depends on receptor-interacting serine-threonine kinase 3 (RIPK3) and mixed lineage kinase domain-like (MLKL) and generally manifests with morphological features of necrosis. The molecular mechanisms that underlie distinct instances of necroptosis have just begun to emerge. Nonetheless, it has already been shown that necroptosis contributes to cellular demise in various pathophysiological conditions, including viral infection, acute kidney injury, and cardiac ischemia/reperfusion. Moreover, human tumors appear to obtain an advantage from the downregulation of key components of the molecular machinery for necroptosis. Although such an advantage may stem from an increased resistance to adverse microenvironmental conditions, accumulating evidence indicates that necroptosis-deficient cancer cells are poorly immunogenic and hence escape natural and therapy-elicited immunosurveillance. Here, we discuss the molecular mechanisms and relevance to disease of necroptosis.

Indexed as

ApoptosisDiseaseNecrosisAnimalsHumansReceptor-Interacting Protein Serine-Threonine KinasesReceptor-Interacting Protein Serine-Threonine KinasesRIPK3 protein, humancaspasesdamage-associated molecular patternsimmunogenic cell deathinflammationmitochondrial permeability transitionnecrostatin-1

Identifiers

PMID27959630
PMCPMC5786374

What OpenQuestion holds

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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.