Evidence map›Paper›PMID 23284892›Full record

ArticlePloS one2012

Myocardial connective tissue growth factor (CCN2/CTGF) attenuates left ventricular remodeling after myocardial infarction.

Jørgen Gravning, Stein Ørn, Ole Jørgen Kaasbøll, Vladimir N Martinov, Cord Manhenke, Kenneth Dickstein, Thor Edvardsen, Håvard Attramadal, Mohammed Shakil Ahmed

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

33 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
  2. Article
  3. The Role of Matrix Proteins in Cardiac Pathology.International journal of molecular sciences · 2022
    Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Extracellular Matrix in Ischemic Heart Disease, Part 4/4: JACC Focus Seminar.Journal of the American College of Cardiology · 2020
    Review
  13. Article
  14. Antiapoptosis and Antifibrosis Effects ofBioMed research international · 2019
    Article
  15. Article
  16. Review
  17. CTGF/CCN2 is an autocrine regulator of cardiac fibrosis.Journal of molecular and cellular cardiology · 2018
    Article
  18. Article
  19. Cardiac fibrosis: new insights into the pathogenesis.International journal of biological sciences · 2018 · on this map
    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 3 institutions in 1 country.

Jørgen GravningInstitute for Surgical Research, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Stein Ørn
Ole Jørgen Kaasbøll
Vladimir N Martinov
Cord Manhenke
Kenneth Dickstein
Thor Edvardsen
Håvard Attramadal
Mohammed Shakil Ahmed
University of Oslo · NOStavanger University Hospital · NOOslo University Hospital · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsMyocardial CCN2/CTGF is induced in heart failure of various etiologies. However, its role in the pathophysiology of left ventricular (LV) remodeling after myocardial infarction (MI) remains unresolved. The current study explores the role of CTGF in infarct healing and LV remodeling in an animal model and in patients admitted for acute ST-elevation MI. METHODS AND

resultsTransgenic mice with cardiac-restricted overexpression of CTGF (Tg-CTGF) and non-transgenic littermate controls (NLC) were subjected to permanent ligation of the left anterior descending coronary artery. Despite similar infarct size (area of infarction relative to area at risk) 24 hours after ligation of the coronary artery in Tg-CTGF and NLC mice, Tg-CTGF mice disclosed smaller area of scar tissue, smaller increase of cardiac hypertrophy, and less LV dilatation and deterioration of LV function 4 weeks after MI. Tg-CTGF mice also revealed substantially reduced mortality after MI. Remote/peri-infarct tissue of Tg-CTGF mice contained reduced numbers of leucocytes, macrophages, and cells undergoing apoptosis as compared with NLC mice. In a cohort of patients with acute ST-elevation MI (n = 42) admitted to hospital for percutaneous coronary intervention (PCI) serum-CTGF levels (s-CTGF) were monitored and related to infarct size and LV function assessed by cardiac MRI. Increase in s-CTGF levels after MI was associated with reduced infarct size and improved LV ejection fraction one year after MI, as well as attenuated levels of CRP and GDF-15.

conclusionIncreased myocardial CTGF activities after MI are associated with attenuation of LV remodeling and improved LV function mediated by attenuation of inflammatory responses and inhibition of apoptosis.

Indexed as

AnimalsApoptosisCardiomegalyConnective Tissue Growth FactorC-Reactive ProteinDisease Models, AnimalFemaleFibrosisGrowth Differentiation Factor 15Heart FailureHumansKi-67 AntigenMaleMiceMice, TransgenicMicrovesselsConnective Tissue Growth FactorC-Reactive ProteinGrowth Differentiation Factor 15Ki-67 AntigenProto-Oncogene Proteins c-kit

Identifiers

PMID23284892
PMCPMC3527406
OpenAlexW2025455757

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.