Evidence map›Paper›PMID 24572254›Full record

ArticleJournal of the American Heart Association2014

Dysferlin mediates the cytoprotective effects of TRAF2 following myocardial ischemia reperfusion injury.

Huei-Ping Tzeng, Sarah Evans, Feng Gao, Kari Chambers, Veli K Topkara, Natarajan Sivasubramanian, Philip M Barger, Douglas L Mann

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

23 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Observational
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Roles of TRAFs in Ischemia-Reperfusion Injury.Frontiers in cell and developmental biology · 2020
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
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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

8 authors at 2 institutions in 1 country.

Huei-Ping TzengCenter for Cardiovascular Research, Division of Cardiology, Department of Medicine, Washington University School of Medicine, St. Louis, MO.
Sarah Evans
Feng Gao
Kari Chambers
Veli K Topkara
Natarajan Sivasubramanian
Philip M Barger
Douglas L Mann
Washington University in St. Louis · USBaylor College of Medicine · US

Funding

PRINCIPLES IN CARDIVASCULAR RESEARCH TRAINING PROGRAMT32HL007081 · NHLBI · WASHINGTON UNIVERSITY · PI Abhinav Diwan, Karen Ellen Joynt Maddox · 1985 to 2026
$10.6M
TRAINING GRANT IN MOLECULAR CARDIOLOGYT32HL007706 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI ENTMAN, MARK L · 1992 to 2008
$2.1M
CYTOPROTECTIVE EFFECTS OF INFLAMMATION MEDIATED MEMBRANE REPAIRR01HL111094 · NHLBI · WASHINGTON UNIVERSITY · PI MANN, DOUGLAS L · 2012 to 2016
$1.9M
Cytoprotective Cytokine Signaling and Reperfusion InjuryR01HL089543 · NHLBI · WASHINGTON UNIVERSITY · PI MANN, DOUGLAS L · 2009 to 2010
$779k
NHLBI NIH HHS R01 HL089543NHLBI NIH HHS R01 HL111094NHLBI NIH HHS R01 HL89543NHLBI NIH HHS T32 HL007081NHLBI NIH HHS T32 HL007706PHS HHS R01 111094
6 · The paper itself

Abstract

backgroundWe have demonstrated that tumor necrosis factor (TNF) receptor-associated factor 2 (TRAF2), a scaffolding protein common to TNF receptors 1 and 2, confers cytoprotection in the heart. However, the mechanisms for the cytoprotective effects of TRAF2 are not known. METHODS/

resultsMice with cardiac-restricted overexpression of low levels of TRAF2 (MHC-TRAF2LC) and a dominant negative TRAF2 (MHC-TRAF2DN) were subjected to ischemia (30-minute) reperfusion (60-minute) injury (I/R), using a Langendorff apparatus. MHC-TRAF2LC mice were protected against I/R injury as shown by a significant ≈27% greater left ventricular (LV) developed pressure after I/R, whereas mice with impaired TRAF2 signaling had a significantly ≈38% lower LV developed pressure, a ≈41% greater creatine kinase (CK) release, and ≈52% greater Evans blue dye uptake after I/R, compared to LM. Transcriptional profiling of MHC-TRAF2LC and MHC-TRAF2DN mice identified a calcium-triggered exocytotic membrane repair protein, dysferlin, as a potential cytoprotective gene responsible for the cytoprotective effects of TRAF2. Mice lacking dysferlin had a significant ≈39% lower LV developed pressure, a ≈20% greater CK release, and ≈29% greater Evans blue dye uptake after I/R, compared to wild-type mice, thus phenocopying the response to tissue injury in the MHC-TRAF2DN mice. Moreover, breeding MHC-TRAF2LC onto a dysferlin-null background significantly attenuated the cytoprotective effects of TRAF2 after I/R injury.

conclusionThe study shows that dysferlin, a calcium-triggered exocytotic membrane repair protein, is required for the cytoprotective effects of TRAF2-mediated signaling after I/R injury.

Indexed as

AnimalsBiomarkersCell Membrane PermeabilityCreatine KinaseDisease Models, AnimalDysferlinGene Expression ProfilingGene Expression RegulationGenotypeMembrane ProteinsMiceMice, 129 StrainMice, KnockoutMice, TransgenicMutationMyocardial Reperfusion InjuryBiomarkersCreatine KinaseDysferlinDysf protein, mouseMembrane ProteinsTNF Receptor-Associated Factor 2cytoprotectiondysferlinTNF receptor associated factor 2tumor necrosis factor

Identifiers

PMID24572254
PMCPMC3959693
OpenAlexW2102228957

What OpenQuestion holds

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LicenceCC BY-NC
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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.