Evidence map›Paper›PMID 20036880›Full record

ArticleFrontiers in bioscience (Elite edition)2010

Ablation of iNOS delays cardiac contractile dysfunction in chronic hypertension.

Fernando A L Dias, Dalia Urboniene, Milana A Yuzhakova, Brandon J Biesiadecki, James R Pena, Paul H Goldspink, David L Geenen, Beata M Wolska

Open access · bronzeAbstract read
In one paragraph

Article in Frontiers in bioscience (Elite edition), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

10 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. The NO/ONOO-cycle as the central cause of heart failure.International journal of molecular sciences · 2013
    Review
  10. Article
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 1 institution in 1 country.

Fernando A L DiasDepartment of Medicine, Section of Cardiology, Center for Cardiovascular Research, University of Illinois at Chicago, IL 60612, USA.
Dalia Urboniene
Milana A Yuzhakova
Brandon J Biesiadecki
James R Pena
Paul H Goldspink
David L Geenen
Beata M Wolska
University of Illinois Chicago · US

Funding

Sarcomeric Modifications and Progressive Cardiac MaladaptationP01HL062426 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI AI, XUN · 2000 to 2020
$42.4M
TRAINING IN CELLULAR SIGNALLING IN THE CARDIOVASCULAR SYT32HL007692 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI SOLARO, R JOHN · 1990 to 2014
$8.5M
Control of Cardiac Function by Calcium and MyofilamentsR01HL079032 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI WOLSKA, BEATA M. · 2005 to 2008
$1.3M
The Role of NO in the Regulation of Heart ContractilityR01HL064209 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI WOLSKA, BEATA M. · 2001 to 2004
$1.2M
Post-translational Modification in Cardiac MuscleR00HL091056 · NHLBI · OHIO STATE UNIVERSITY · PI BIESIADECKI, BRANDON J · 2009 to 2011
$747k
The Role of Tropomyosin Post-translational Modification in Cardiac MuscleK99HL091056 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI BIESIADECKI, BRANDON J · 2008 to 2009
$180k
NHLBI NIH HHS HL64209NHLBI NIH HHS HL79032NHLBI NIH HHS HL91056NHLBI NIH HHS K99 HL091056NHLBI NIH HHS P01 HL062426NHLBI NIH HHS R00 HL091056NHLBI NIH HHS R01 HL064209NHLBI NIH HHS R01 HL079032NHLBI NIH HHS T32 HL007692NHLBI NIH HHS T32HL07692PHS HHS P01-62426
6 · The paper itself

Abstract

We investigated the role of inducible NOS (iNOS) on cardiac function during the development of left ventricular hypertrophy. Hypertrophy was induced by pressure-overload via short-term (2.5 months) or long-term (6.5 months) aortic banding (AoB) in wild-type (WT) and iNOS knock out (iNOSKO) mice. Cardiac function was then assessed via echocardiography, in situ hemodynamics and papillary muscle force measurements. Quantitative RT-PCR and Western blots were used to measure expression of hypertrophic gene markers and proteins respectively. Our data demonstrate that increased afterload via AoB leads to increased expression of iNOS that is associated with cardiac dysfunction. In pressure-overload induced hypertrophy, iNOSKO delays both the expression of hypertrophic markers and contractile dysfunction without causing significant changes in the level of hypertrophy. Moreover, after long-term AoB, iNOSKO animals exhibited increased basal cardiac function and an improved response to beta-adrenergic stimulation compared to long-term AoB WT animals. In conclusion, our data demonstrate that NO production via iNOS plays an important role in modulating cardiac function after moderate AoB that mimics long-term hypertension in humans.

Indexed as

Analysis of VarianceAnimalsAortaBiomarkersBlotting, WesternEchocardiographyFluorescent Antibody TechniqueHemodynamicsHypertensionHypertrophy, Left VentricularLigationMaleMiceMyocardial ContractionMyosin Heavy ChainsNitric Oxide Synthase Type IIBiomarkersMyosin Heavy ChainsNitric Oxide Synthase Type IINitric Oxide Synthase Type IIINos2 protein, mouseNos3 protein, mouse

Identifiers

PMID20036880
PMCPMC2901916
OpenAlexW1678567907

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.