Evidence map›Paper›PMID 25148874›Full record

ArticleMolecular and cellular biochemistry2014

Platelet-derived growth factor blockade on cardiac remodeling following infarction.

Chang Liu, Wenyuan Zhao, Weixin Meng, Tieqiang Zhao, Yuanjian Chen, Robert A Ahokas, Hongyu Liu, Yao Sun

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular and cellular biochemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

25 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Signaling Pathways and Potential Therapeutic Strategies in Cardiac Fibrosis.International journal of molecular sciences · 2023
    Review
  5. Article
  6. The Pathogenesis of Cardiac Fibrosis: A Review of Recent Progress.International journal of molecular sciences · 2022
    Review
  7. Article
  8. Article
  9. Article
  10. Cardiac fibrosis.Cardiovascular research · 2021
    Review
  11. Article
  12. Review
  13. Emerging imaging targets for infiltrative cardiomyopathy: Inflammation and fibrosis.Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology · 2019
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  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

8 authors at 3 institutions in 2 countries.

Chang LiuDivision of Cardiac Surgery, Department of Surgery, The First Affiliate Hospital of Harbin Medical University, Harbin, China.
Wenyuan Zhao
Weixin Meng
Tieqiang Zhao
Yuanjian Chen
Robert A Ahokas
Hongyu Liu
Yao Sun
University of Tennessee Health Science Center · USFirst Affiliated Hospital of Harbin Medical University · CNHarbin Medical University · CN

Funding

Regulatory Mechanisms of Oxidative Stress in Cardiac Angiogenesis PostinfarctionR01HL096503 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI SUN, YAO · 2010 to 2013
$1.5M
NHLBI NIH HHS 1R01-HL096503NHLBI NIH HHS R01 HL096503
6 · The paper itself

Abstract

Cardiac repair and remodeling occur following myocardial infarction (MI). Our previous study demonstrated that platelet-derived growth factor (PDGF)-A/-D and PDGF receptors (PDGFR) are increased in the infarcted heart, with cells expressing PDGFR primarily endothelial and fibroblast-like cells. In the present study, we tested the hypothesis that PDGF contributes to cardiac angiogenesis and fibrogenesis post-MI. Rats with experimental MI were treated with either a PDGFR antagonist (Imatinib, 40 mg/kg/day) or vehicle by gavage, and sham-operated rats served as the controls. Cardiac fibrogenesis, angiogenesis, and ventricular function were detected at weeks 1 and 4 post-MI. We found that (1) transforming growth factor (TGF)-β1, tissue inhibitors of metalloproteinases (TIMP)-1/-2, and type I collagen mRNA were all significantly increased in the infarcted heart at week 1 post-MI, while PDGFR blockade significantly reduced these fibrogenic mediators in the noninfarcted myocardium as compared to controls; (2) fibrosis developed in both the infarcted and noninfarcted myocardium at week 4 with PDGFR blockade significantly suppressing collagen volume in the noninfarcted myocardium; (3) angiogenesis was activated in the infarcted myocardium, particularly at week 1, and was not altered by treatment with imatinib; and (4) ventricular dysfunction was evident in MI rats at week 4, and mildly improved with imatinib treatment. These observations indicated that PDGF can contribute to the development of cardiac interstitial fibrosis in the noninfarcted myocardium, but does not alter scar formation in the infarcted myocardium. Further, this study suggests the potential therapeutic effects of PDGFR blockade on interstitial fibrosis of the infarcted heart.

Indexed as

AnimalsBenzamidesFibrosisImatinib MesylateLymphokinesMaleMyocardial InfarctionPiperazinesPlatelet-Derived Growth FactorProtein Kinase InhibitorsPyrimidinesRatsRats, Sprague-DawleyReceptors, Platelet-Derived Growth FactorTissue Inhibitor of Metalloproteinase-1Tissue Inhibitor of Metalloproteinase-2BenzamidesImatinib MesylateLymphokinesPdgfd protein, ratPiperazinesPlatelet-Derived Growth Factorplatelet-derived growth factor AProtein Kinase InhibitorsPyrimidinesReceptors, Platelet-Derived Growth FactorTgfb1 protein, ratTIMP1 protein, ratTissue Inhibitor of Metalloproteinase-1Tissue Inhibitor of Metalloproteinase-2Transforming Growth Factor beta1

Identifiers

PMID25148874
OpenAlexW2153805086

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.