Evidence map›Paper›PMID 20938722›Full record

ArticleMolecular and cellular biochemistry2011

Myocardial fibrosis and TGFB expression in hyperhomocysteinemic rats.

Lamia Raaf, Christophe Noll, Mohamed El Hadi Cherifi, Jane-Lise Samuel, Claude Delcayre, Jean-Maurice Delabar, Yasmina Benazzoug, Nathalie Janel

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular and cellular biochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

15 citing papers in PubMed, 33 citations in OpenAlex.

  1. Atherogenic Effect of Homocysteine, a Biomarker of Inflammation and Its Treatment.The International journal of angiology : official publication of the International College of Angiology, Inc · 2024
    Review
  2. Dual optical elastography detectsJournal of biomedical optics · 2024
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. IntermedinJournal of atherosclerosis and thrombosis · 2016
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. 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 5 institutions in 2 countries.

Lamia RaafUniv Paris Diderot-CNRS EAC 4413, unité de Biologie Fonctionnelle et Adaptative, Case 7104, 75205, Paris cedex 13, France.
Christophe Noll
Mohamed El Hadi Cherifi
Jane-Lise Samuel
Claude Delcayre
Jean-Maurice Delabar
Yasmina Benazzoug
Nathalie Janel
Université Paris Cité · FRCentre National de la Recherche Scientifique · FRCentre de Recherche Nucléaire d’Alger · DZHôpital Lariboisière · FRUniversity of Sciences and Technology Houari Boumediene · DZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hyperhomocysteinemia, characterized by an elevated plasma homocysteine concentration, leads to several clinical manifestations and particularly cardiovascular diseases. Experimental models of hyperhomocysteinemia revealed several tissue injuries including heart fibrosis and ventricular hypertrophy. In order to analyze the molecular mechanisms link to these morphological alterations, a mild hyperhomocysteinemia was induced in rats via a chronic methionine administration. Effects of methionine administration were examined by histological analysis with Sirius red staining, histomorphometric analysis, zymography, and immunoblotting. Hyperhomocysteinemia due to methionine administration produces an interstitial myocardial fibrosis and a ventricular cardiomyocyte hypertrophy, which were associated with increased expression of transforming growth factor-beta1 (TGFβ1), tissue inhibitors of metalloproteinase (TIMP) 2, and JNK activation. However, the matrix metalloproteinase 2 activity was decreased in the hearts of hyperhomocysteinemic rats. Moreover, the TIMP1 protein expression was decreased, and the TIMP1-MMP1 balance was shifted. Remodeling in cardiac tissue observed in rat model of mild hyperhomocysteinemia is associated with a dysregulation in extracellular matrix degradation which results, at least in part, from enhancement of TGFβ1 level.

Indexed as

AnimalsCollagenEnzyme ActivationExtracellular MatrixFibrosisHomocysteineHyperhomocysteinemiaJNK Mitogen-Activated Protein KinasesMaleMatrix Metalloproteinase 1Matrix Metalloproteinase 3MyocardiumMyocytes, CardiacRatsRats, WistarTime FactorsCollagenHomocysteineJNK Mitogen-Activated Protein KinasesMatrix Metalloproteinase 1Matrix Metalloproteinase 3Tgfb1 protein, ratTissue Inhibitor of Metalloproteinase-1Transforming Growth Factor beta1

Identifiers

PMID20938722
OpenAlexW1984393180

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.