Evidence map›Paper›PMID 31391333›Full record

ReviewJCI insight2019

Necroptosis: a crucial pathogenic mediator of human disease.

Mary E Choi, David R Price, Stefan W Ryter, Augustine M K Choi

Open access · goldAbstract readReview
In one paragraph

Review in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 245 papers.

0numbers the graph read from it
0cells of the map it votes in
245citing papers in PubMed
18.2field-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

245 citing papers in PubMed, 421 citations in OpenAlex.

  1. Review
  2. Article
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  11. Review
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  17. Review
  18. Article
  19. Induced necroptosis limitsInfection and immunity · 2025
    Article
  20. Review

185 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 3 institutions in 1 country.

Mary E ChoiDivision of Nephrology and Hypertension, Joan and Sanford I. Weill Department of Medicine, Weill Cornell Medicine, New York, New York, USA.
David R PriceNewYork-Presbyterian Hospital, Weill Cornell Medical Center, New York, New York, USA.
Stefan W RyterDivision of Pulmonary and Critical Care Medicine, Joan and Sanford I. Weill Department of Medicine, Weill Cornell Medicine, New York, New York, USA.
Augustine M K ChoiNewYork-Presbyterian Hospital, Weill Cornell Medical Center, New York, New York, USA.
Weill Cornell Medicine · USNew York Hospital Queens · USNewYork–Presbyterian Hospital · US

Funding

Disparities in COVID Disease Severity and Outcomes in New York CityUL1TR002384 · NCATS · WEILL MEDICAL COLL OF CORNELL UNIV · PI JULIANNE L IMPERATO-MCGINLEY · 2017 to 2026
$86.2M
Clinical and Translational Science CenterUL1TR000457 · NCATS · WEILL MEDICAL COLL OF CORNELL UNIV · PI IMPERATO-MCGINLEY, JULIANNE L · 2012 to 2016
$46.0M
Respiratory Computational Discovery CoreP01HL114501 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI CHOI, MARY E · 2013 to 2025
$24.9M
The Role of HEME Oxygenase in Hyperoxic Lung InjuryR01HL055330 · NHLBI · YALE UNIVERSITY · PI CHOI, AUGUSTINE M, CHOI, MARY E · 1998 to 2021
$6.6M
Multidisciplinary Approach Training in Respiratory ResearchT32HL134629 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI Robert J Kaner, Heather Winona Stout Delgado · 2018 to 2026
$5.2M
Metabolic dysfunction regulates mitophagy-dependent necroptosis in COPDR01HL132198 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI CHOI, AUGUSTINE M, CHOI, MARY E · 2017 to 2020
$2.2M
Novel role of RIPK3-dependent necroptosis pathway in lung and kidney fibrosisR01HL133801 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI CHOI, AUGUSTINE M, CHOI, MARY E · 2017 to 2020
$2.1M
NCATS NIH HHS UL1 TR000457NCATS NIH HHS UL1 TR002384NHLBI NIH HHS P01 HL114501NHLBI NIH HHS R01 HL055330NHLBI NIH HHS R01 HL132198NHLBI NIH HHS R01 HL133801NHLBI NIH HHS T32 HL134629
6 · The paper itself

Abstract

Necroptosis is a genetically regulated form of necrotic cell death that has emerged as an important pathway in human disease. The necroptosis pathway is induced by a variety of signals, including death receptor ligands, and regulated by receptor-interacting protein kinases 1 and 3 (RIPK1 and RIPK3) and mixed-lineage kinase domain-like pseudokinase (MLKL), which form a regulatory necrosome complex. RIPK3-mediated phosphorylation of MLKL executes necroptosis. Recent studies, using animal models of tissue injury, have revealed that RIPK3 and MLKL are key effectors of injury propagation. This Review explores the functional roles of RIPK3 and MLKL as crucial pathogenic determinants and markers of disease progression and severity in experimental models of human disease, including acute and chronic pulmonary diseases; renal, hepatic, cardiovascular, and neurodegenerative diseases; cancer; and critical illness.

Indexed as

NecroptosisAnimalsCardiovascular DiseasesDisease Models, AnimalDisease ProgressionHumansKidney DiseasesLiver DiseasesLung DiseasesNeoplasmsNeurodegenerative DiseasesPhosphorylationProtein KinasesReceptor-Interacting Protein Serine-Threonine KinasesMLKL protein, humanProtein KinasesReceptor-Interacting Protein Serine-Threonine KinasesRIPK1 protein, humanRIPK3 protein, human

Identifiers

PMID31391333
PMCPMC6693822
OpenAlexW2965244259

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.