Evidence map›Paper›PMID 28462521›Full record

ReviewImmunological reviews2017

RIPK3 in cell death and inflammation: the good, the bad, and the ugly.

Susana Orozco, Andrew Oberst

Abstract readReview
In one paragraph

Review in Immunological reviews, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

78 citing papers in PubMed, 115 citations in OpenAlex.

  1. Evaluating Intermittent Dosing of Aspirin for Colorectal Cancer Chemoprevention.Cancer prevention research (Philadelphia, Pa.) · 2025
    Trial
  2. Review
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  11. A viral necrosome mediates direct RIPK3 activation to promote inflammatory necroptosis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  12. Article
  13. Article
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  16. RIP3 regulates doxorubicin-induced intestinal mucositis via FUT2-mediated α-1,2-fucosylation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Article
  17. Review
  18. Review
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18 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

2 authors at 1 institution in 3 countries.

Susana OrozcoDepartment of Immunology, University of Washington, Seattle, WA, USA.
Andrew OberstDepartment of Immunology, University of Washington, Seattle, WA, USA.ORCID 0000-0002-9500-7912
University of Washington · US

Funding

The physiological role of RIPK3-dependent necroptosisR01AI108685 · NIAID · UNIVERSITY OF WASHINGTON · PI OBERST, ANDREW ATWELL · 2014 to 2018
$2.5M
Basic Training at the Intersection of Innate and Adaptive Immunity in DiseaseT32AI106677 · NIAID · UNIVERSITY OF WASHINGTON · PI GALE, MICHAEL, GOVERMAN, JOAN M · 2013 to 2022
$2.1M
A death-independent function for RIPK3 signaling in neuroinflammationR21NS101542 · NINDS · UNIVERSITY OF WASHINGTON · PI OBERST, ANDREW ATWELL · 2017 to 2018
$483k
Inducing Immunogenic Cell Death In CancerR21CA185681 · NCI · UNIVERSITY OF WASHINGTON · PI OBERST, ANDREW ATWELL · 2015 to 2016
$416k
NCI NIH HHS R21 CA185681NIAID NIH HHS R01 AI108685NIAID NIH HHS T32 AI106677NINDS NIH HHS R21 NS101542
6 · The paper itself

Abstract

Necroptosis is a form of cell death that can be observed downstream of death receptor or pattern recognition receptor signaling under certain cellular contexts, or in response to some viral and bacterial infections. The receptor interacting protein kinases-1 (RIPK1) and RIPK3 are at the core of necroptotic signaling, among other proteins. Because this pathway is normally halted by the pro-apoptotic protease caspase-8 and the IAP ubiquitin ligases, how and when necroptosis is triggered in physiological settings are ongoing questions. Interestingly, accumulating evidence suggests that RIPK3 has functions beyond the induction of necroptotic cell death, especially in the areas of tissue injury and sterile inflammation. Here, we will discuss the role of RIPK3 in a variety of physiological conditions, including necroptotic and non-necroptotic cell death, in the context of viral and bacterial infections, tissue damage, and inflammation.

Indexed as

AnimalsApoptosisBacterial InfectionsDNA Degradation, NecroticHumansInflammationNecrosisReceptor-Interacting Protein Serine-Threonine KinasesReceptors, Death DomainReceptors, Pattern RecognitionSignal TransductionVirus DiseasesReceptor-Interacting Protein Serine-Threonine KinasesReceptors, Death DomainReceptors, Pattern RecognitionRIPK3 protein, humancell deathinfectioninflammationnecroptosisRIPK3tissue damage

Identifiers

PMID28462521
PMCPMC5419046
OpenAlexW2610633818

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.