Evidence map›Paper›PMID 27430031›Full record

ArticleJACC. Basic to translational science2016

Follistatin like 1 Regulates Hypertrophy in Heart Failure with Preserved Ejection Fraction.

Komei Tanaka, María Valero-Muñoz, Richard M Wilson, Eric E Essick, Conor T Fowler, Kazuto Nakamura, Maurice van den Hoff, Noriyuki Ouchi, Flora Sam

Open access · goldAbstract read
In one paragraph

Article in JACC. Basic to translational science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 2 pooled it
3.1field-weighted citation impact, top 8% 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

50 citing papers in PubMed, 2 syntheses or guidelines pooled it, 58 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Skeletal Muscle as Endocrine Organ.Advances in experimental medicine and biology · 2025
    Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Adipokines and Their Role in Heart Failure: A Literature Review.The Journal of innovations in cardiac rhythm management · 2023
    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 3 countries.

Komei Tanaka *Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, USA.
María Valero-Muñoz *Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, USA.
Richard M WilsonWhitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, USA.
Eric E EssickWhitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, USA.
Conor T FowlerWhitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, USA.
Kazuto NakamuraWhitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, USA.
Maurice van den HoffAcademic Medical Center, Heart Failure Research Center, Department of Anatomy, Embryology & Physiology, Amsterdam, The Netherlands.
Noriyuki OuchiDepartment of Molecular Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Flora SamWhitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, USA.
Boston University · USAcademic Medical Center · NLNagoya University · JP

Funding

Role of Aldosterone and Adiponectin in Inter-Tissue Communication in Diastolic HeR01HL117153 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI SAM, FLORA · 2013 to 2016
$1.6M
NHLBI NIH HHS R01 HL117153
6 · The paper itself

Abstract

objectiveWe sought to determine whether Fstl1 plays a role in the regulation of cardiac hypertrophy in HFpEF.

backgroundHeart failure (HF) with METHODS AND

resultsIn this study, blood levels of Fstl1 were increased in humans with HFpEF. This increase was also evident in mice with hypertension-induced HFpEF and adult rat ventricular myocytes stimulated with aldosterone. Treatment with recombinant Fstl1 abrogated aldosterone-induced cardiac myocyte hypertrophy, suggesting a role for Fstl1 in the regulation of hypertrophy in HFpEF. There was also a reduction in the E/A ratio, a measure of diastolic dysfunction. Furthermore, HFpEF induced in a mouse model that specifically ablates Fstl1 in cardiac myocytes (cFstl1-KO), showed exacerbation of HFpEF with worsened diastolic dysfunction. In addition, cFstl1-KO-HFpEF mice demonstrated more marked cardiac myocyte hypertrophy with increased molecular markers of anp and bnp expression.

conclusionsThese findings indicate that Fstl1exerts therapeutic effects by modulating cardiac hypertrophy in HFpEF.

Indexed as

cardiac hypertrophyfollistatin like 1heart failure with preserved ejection fraction

Identifiers

PMID27430031
PMCPMC4944656
OpenAlexW2473248170

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.