Evidence map›Paper›PMID 22915069›Full record

ArticleJournal of cardiovascular translational research2012

Follistatin-like 3 mediates paracrine fibroblast activation by cardiomyocytes.

Kalyani D Panse, Leanne E Felkin, Marina M López-Olañeta, Jesús Gómez-Salinero, María Villalba, Lucía Muñoz, Kazuto Nakamura, Masayuki Shimano, Kenneth Walsh, Paul J R Barton and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of cardiovascular translational research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 19% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Observational
  6. Review
  7. Article
  8. Article
  9. Article
  10. Characterization of a robust mouse model of heart failure with preserved ejection fraction.American journal of physiology. Heart and circulatory physiology · 2023
    Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Cardiac fibrosis.Cardiovascular research · 2021
    Review
  16. Article
  17. The Role of the TGF-β Superfamily in Myocardial Infarction.Frontiers in cardiovascular medicine · 2019
    Review
  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

12 authors at 6 institutions in 4 countries.

Kalyani D PanseHeart Science Centre, Imperial College London, Hill End Road, Middlesex, UB9 6JH, UK.
Leanne E Felkin
Marina M López-Olañeta
Jesús Gómez-Salinero
María Villalba
Lucía Muñoz
Kazuto Nakamura
Masayuki Shimano
Kenneth Walsh
Paul J R Barton
Nadia Rosenthal
Enrique Lara-Pezzi
Spanish National Centre for Cardiovascular Research · ESImperial College London · GBBoston Medical Center · USAustralian Regenerative Medicine Institute · AUBoston University · USRoyal Brompton & Harefield NHS Foundation Trust · GB

Funding

British Heart Foundation PG/08/084/25827
6 · The paper itself

Abstract

Follistatins are extracellular inhibitors of the TGF-β family ligands including activin A, myostatin and bone morphogenetic proteins. Follistatin-like 3 (FSTL3) is a potent inhibitor of activin signalling and antagonises the cardioprotective role of activin A in the heart. FSTL3 expression is elevated in patients with heart failure and is upregulated in cardiomyocytes by hypertrophic stimuli, but its role in cardiac remodelling is largely unknown. Here, we show that the production of FSTL3 by cardiomyocytes contributes to the paracrine activation of cardiac fibroblasts, inducing changes in cell adhesion, promoting proliferation and increasing collagen production. We found that FSTL3 is necessary for this response and for the induction of cardiac fibrosis. However, full activation requires additional factors, and we identify connective tissue growth factor as a FSTL3 binding partner in this process. Together, our data unveil a novel mechanism of paracrine communication between cardiomyocytes and fibroblasts that may provide potential as a therapeutic target in heart remodelling.

Indexed as

Paracrine CommunicationAnimalsCell AdhesionCell ProliferationCells, CulturedCoculture TechniquesCollagenConnective Tissue Growth FactorDisease Models, AnimalFibroblastsFibrosisFollistatin-Related ProteinsGene Expression RegulationHeart FailureHumansMiceCollagenConnective Tissue Growth FactorFollistatin-Related ProteinsFstl3 protein, mouseProteins

Identifiers

PMID22915069
OpenAlexW2032443543

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.