Evidence map›Paper›PMID 19364763›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2009

Beta3 integrin-mediated ubiquitination activates survival signaling during myocardial hypertrophy.

Rebecca K Johnston, Sundaravadivel Balasubramanian, Harinath Kasiganesan, Catalin F Baicu, Michael R Zile, Dhandapani Kuppuswamy

Abstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

40 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
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  3. Article
  4. Article
  5. Review
  6. Review
  7. Targeting integrin pathways: mechanisms and advances in therapy.Signal transduction and targeted therapy · 2023
    Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Cardioprotection of an IAmerican journal of translational research · 2021
    Article
  13. Review
  14. Article
  15. Article
  16. Article
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  18. 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

6 authors at 2 institutions in 1 country.

Rebecca K JohnstonCardiology Division of the Department of Medicine, Gazes Cardiac Research Institute, Medical University of South Carolina, Charleston, South Carolina 29425-2221, USA.
Sundaravadivel Balasubramanian
Harinath Kasiganesan
Catalin F Baicu
Michael R Zile
Dhandapani Kuppuswamy
Medical University of South Carolina · USRalph H. Johnson VA Medical Center · US

Funding

TRANSLATIONAL REGULATION OF CARDIAC PROTEIN SYNTHESISP01HL048788 · NHLBI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI COOPER, GEORGE · 1993 to 2007
$15.9M
TRAINING TO IMPROVE CARDIOVASCULAR THERAPIEST32HL007260 · NHLBI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI MENICK, DONALD R. · 1985 to 2021
$11.1M
mTOR in Growth and Protection of Hypertrophying MyocardiumR01HL092124 · NHLBI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI KUPPUSWAMY, DHANDAPANI · 2009 to 2012
$1.5M
NHLBI NIH HHS HL-48788NHLBI NIH HHS P01 HL048788NHLBI NIH HHS R01 HL-092124NHLBI NIH HHS R01 HL092124NHLBI NIH HHS T32 HL007260NHLBI NIH HHS T32HL07260
6 · The paper itself

Abstract

Identifying the molecular mechanisms activated in compensatory hypertrophy and absent during decompensation will provide molecular targets for prevention of heart failure. We have previously shown enhanced ubiquitination (Ub) during the early growth period of pressure overload (PO) hypertrophy near intercalated discs of cardiomyocytes, where integrins are important for mechanotransduction. In this study, we tested the role of integrins upstream of Ub, whether enhanced Ub contributes to survival signaling in early PO, and if loss of this mechanism could lead to decreased ventricular function. The study used a beta(3) integrin (-/-) mouse and a wild-type mouse as a control for in vivo PO by transverse aortic constriction (TAC) and for cultured cardiomyocytes in vitro, stimulated with the integrin-activating peptide RGD. We demonstrate beta(3) integrin mediates transient Ub of targeted proteins during PO hypertrophy, which is necessary for cardiomyocyte survival and to maintain ventricular function. Prosurvival signaling proceeds by initiation of NF-kappaB transcription of the E3 ligase, cIAP1. In PO beta(3)(-/-) mice, absence of this mechanism correlates with increased TUNEL staining and decreased ventricular mass and function by 4 wk. This is the first study to show that a beta(3) integrin/Ub/NF-kappaB pathway contributes to compensatory hypertrophic growth.

Indexed as

AnimalsCardiomegalyCatsCells, CulturedCell SurvivalI-kappa B ProteinsInhibitor of Apoptosis ProteinsIntegrin beta3MiceMice, Inbred C57BLMice, KnockoutModels, CardiovascularMyocytes, CardiacNF-kappa BOligopeptidesSignal Transductionarginyl-glycyl-aspartic acidI-kappa B ProteinsInhibitor of Apoptosis ProteinsIntegrin beta3NF-kappa BOligopeptides

Identifiers

PMID19364763
PMCPMC2717769
OpenAlexW2172266317

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.