Evidence map›Paper›PMID 28572508›Full record

ArticleCirculation2017

Cardioprotective Role of Tumor Necrosis Factor Receptor-Associated Factor 2 by Suppressing Apoptosis and Necroptosis.

Xiaoyun Guo, Haifeng Yin, Lei Li, Yi Chen, Jing Li, Jessica Doan, Rachel Steinmetz, Qinghang Liu

Open access · greenAbstract read
In one paragraph

Article in Circulation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

70 citing papers in PubMed, 95 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Apoptosis in Cardiac Conditions Including Cirrhotic Cardiomyopathy.International journal of molecular sciences · 2025
    Review
  8. Article
  9. Programmed cardiomyocyte death in myocardial infarction.Apoptosis : an international journal on programmed cell death · 2025
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

10 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Xiaoyun GuoFrom Department of Physiology and Biophysics, University of Washington, Seattle.
Haifeng YinFrom Department of Physiology and Biophysics, University of Washington, Seattle.
Lei LiFrom Department of Physiology and Biophysics, University of Washington, Seattle.
Yi ChenFrom Department of Physiology and Biophysics, University of Washington, Seattle.
Jing LiFrom Department of Physiology and Biophysics, University of Washington, Seattle.
Jessica DoanFrom Department of Physiology and Biophysics, University of Washington, Seattle.
Rachel SteinmetzFrom Department of Physiology and Biophysics, University of Washington, Seattle.
Qinghang LiuFrom Department of Physiology and Biophysics, University of Washington, Seattle. qcliu@u.washington.edu.
University of Washington · US

Funding

CARDIOVASCULAR RESEARCH TRAINING PROGRAMT32HL007828 · NHLBI · UNIVERSITY OF WASHINGTON · PI Francis Kim, Farid Moussavi-Harami · 1997 to 2026
$10.2M
A Critical TAK1 Signaling Network in Myocardial Survival and RemodelingR01HL116507 · NHLBI · UNIVERSITY OF WASHINGTON · PI LIU, QINGHANG · 2013 to 2017
$1.9M
Role of TAK1 Signaling Network in Cardiac HypertrophyR00HL098076 · NHLBI · UNIVERSITY OF WASHINGTON · PI LIU, QINGHANG · 2011 to 2013
$735k
NHLBI NIH HHS R00 HL098076NHLBI NIH HHS R01 HL116507NHLBI NIH HHS T32 HL007828
6 · The paper itself

Abstract

backgroundProgrammed cell death, including apoptosis, mitochondria-mediated necrosis, and necroptosis, is critically involved in ischemic cardiac injury, pathological cardiac remodeling, and heart failure progression. Whereas apoptosis and mitochondria-mediated necrosis signaling is well established, the regulatory mechanisms of necroptosis and its significance in the pathogenesis of heart failure remain elusive.

methodsWe examined the role of tumor necrosis factor receptor-associated factor 2 (Traf2) in regulating myocardial necroptosis and remodeling using genetic mouse models. We also performed molecular and cellular biology studies to elucidate the mechanisms by which Traf2 regulates necroptosis signaling.

resultsWe identified a critical role for Traf2 in myocardial survival and homeostasis by suppressing necroptosis. Cardiac-specific deletion of

conclusionsThese results identify an important Traf2-mediated, NFκB-independent, prosurvival pathway in the heart by suppressing necroptotic signaling, which may serve as a new therapeutic target for pathological remodeling and heart failure.

Indexed as

AnimalsAnimals, NewbornApoptosisCardiotonic AgentsCell DeathCells, CulturedMiceMice, KnockoutMice, TransgenicMyocytes, CardiacNecrosisRatsRats, Sprague-DawleyTNF Receptor-Associated Factor 2Ventricular RemodelingCardiotonic AgentsTNF Receptor-Associated Factor 2TRAF2 protein, mousecardiomyocyteheart failurenecroptosispathological remodelingsignal transduction

Identifiers

PMID28572508
PMCPMC5568494
OpenAlexW2621068719

What OpenQuestion holds

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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.