Evidence map›Paper›PMID 23582094›Full record

ArticleJournal of cardiac failure2013

Regulation of connective tissue growth factor gene expression and fibrosis in human heart failure.

Yevgeniya E Koshman, Nilamkumar Patel, Miensheng Chu, Rekha Iyengar, Taehoon Kim, Cagatay Ersahin, William Lewis, Alain Heroux, Allen M Samarel

Open access · greenAbstract read
In one paragraph

Article in Journal of cardiac failure, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

32 citing papers in PubMed, 66 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Epigenetics in Heart Failure.International journal of molecular sciences · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. The Pathogenesis of Cardiac Fibrosis: A Review of Recent Progress.International journal of molecular sciences · 2022
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Mechanisms of cardiac collagen deposition in experimental models and human disease.Translational research : the journal of laboratory and clinical medicine · 2019
    Review
  16. Intervention Mechanisms of Xinmailong Injection, aEvidence-based complementary and alternative medicine : eCAM · 2019
    Review
  17. Article
  18. Article
  19. Review
  20. 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

9 authors at 2 institutions in 1 country.

Yevgeniya E KoshmanDepartment of Medicine, Stritch School of Medicine, Loyola University Chicago, Maywood, IL, USA.
Nilamkumar Patel
Miensheng Chu
Rekha Iyengar
Taehoon Kim
Cagatay Ersahin
William Lewis
Alain Heroux
Allen M Samarel
Loyola University Chicago · USEmory University · US

Funding

Sarcomeric Modifications and Progressive Cardiac MaladaptationP01HL062426 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI AI, XUN · 2000 to 2020
$42.4M
Novel Approaches in Treatment of Vascular Injury Following Balloon AngioplastyF32HL096143 · NHLBI · LOYOLA UNIVERSITY CHICAGO · PI KOSHMAN, YEVGENIYA EMRE · 2010 to 2013
$128k
NHLBI NIH HHS F32 HL096143NHLBI NIH HHS IF32 HL096143NHLBI NIH HHS P01 HL062426NHLBI NIH HHS P01 HL62426
6 · The paper itself

Abstract

backgroundHeart failure (HF) is associated with excessive extracellular matrix (ECM) deposition and abnormal ECM degradation leading to cardiac fibrosis. Connective tissue growth factor (CTGF) modulates ECM production during inflammatory tissue injury, but available data on CTGF gene expression in failing human heart and its response to mechanical unloading are limited. METHODS AND

resultsLeft ventricle (LV) tissue from patients undergoing cardiac transplantation for ischemic (ICM; n = 20) and dilated (DCM; n = 20) cardiomyopathies and from nonfailing (NF; n = 20) donor hearts were examined. Paired samples (n = 15) from patients undergoing LV assist device (LVAD) implantation as "bridge to transplant" (34-1,145 days) also were analyzed. There was more interstitial fibrosis in both ICM and DCM compared with NF hearts. Hydroxyproline concentration was also significantly increased in DCM compared with NF samples. The expression of CTGF, transforming growth factor (TGF) β1, collagen (COL) 1-α1, COL3-α1, matrix metalloproteinase (MMP) 2, and MMP9 mRNA in ICM and DCM were also significantly elevated compared with NF samples. Although TGF-β1, CTGF, COL1-α1, and COL3-α1 mRNA levels were reduced by unloading, there was only a modest reduction in tissue fibrosis and no difference in protein-bound hydroxyproline concentration between pre- and post-LVAD tissue samples. The persistent fibrosis may be related to a concomitant reduction in MMP9 mRNA and protein levels following unloading.

conclusionsCTGF may be a key regulator of fibrosis during maladaptive remodeling and progression to HF. Although mechanical unloading normalizes most genotypic and functional abnormalities, its effect on ECM remodeling during HF is incomplete.

Indexed as

Gene Expression RegulationHeart TransplantationCardiomyopathy, DilatedConnective Tissue Growth FactorFibrosisHeart FailureHumansVentricular RemodelingCCN2 protein, humanConnective Tissue Growth Factor

Identifiers

PMID23582094
PMCPMC3643143
OpenAlexW2146415392

What OpenQuestion holds

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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.