Evidence map›Paper›PMID 21987816›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2011

Cardiac myocyte follistatin-like 1 functions to attenuate hypertrophy following pressure overload.

Masayuki Shimano, Noriyuki Ouchi, Kazuto Nakamura, Bram van Wijk, Koji Ohashi, Yasuhide Asaumi, Akiko Higuchi, David R Pimentel, Flora Sam, Toyoaki Murohara and 2 more

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed, 2 pooled it
2.4field-weighted citation impact, top 11% 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

80 citing papers in PubMed, 2 syntheses or guidelines pooled it, 136 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Follistatin like-1 (Adipocyte · 2024
    Article
  17. Article
  18. Article
  19. Modified mRNA Therapeutics for Heart Diseases.International journal of molecular sciences · 2022
    Review
  20. Review

20 more citing papers are in PubMed but not listed here.

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 3 institutions in 3 countries.

Masayuki ShimanoWhitaker Cardiovascular Institute, Boston University, Boston, MA 02118, USA.
Noriyuki Ouchi
Kazuto Nakamura
Bram van Wijk
Koji Ohashi
Yasuhide Asaumi
Akiko Higuchi
David R Pimentel
Flora Sam
Toyoaki Murohara
Maurice J B van den Hoff
Kenneth Walsh
Boston University · USAcademic Medical Center · NLNagoya University · JP

Funding

SIRT1, Polyphenols, and Endothelial OxidantsP01HL068758 · NHLBI · BOSTON MEDICAL CENTER · PI WALSH, KENNETH · 2003 to 2013
$14.1M
REGULATION OF VESSEL WALL APOPTOSISR37AG015052 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI WALSH, KENNETH · 2003 to 2012
$4.0M
Muscle loss and metabolic dysfunction associated with agingR01AG034972 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI WALSH, KENNETH · 2010 to 2014
$1.6M
Paracrine Regulation of Heart FailureR01HL116591 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI WALSH, KENNETH · 2013 to 2016
$1.6M
REGULATION OF VESSEL WALL APOPTOSISR01AG015052 · NIA · CARITAS ST. ELIZABETH'S MEDICAL CENTER · PI WALSH, KENNETH · 1998 to 2002
$1.0M
Mitochondrial Fusion and Cardiac FunctionR21HL102874 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI WALSH, KENNETH · 2010 to 2011
$448k
NHLBI NIH HHS HL102874NHLBI NIH HHS HL68758NHLBI NIH HHS P01 HL068758NHLBI NIH HHS R01 HL116591NHLBI NIH HHS R21 HL102874NIA NIH HHS AG15052NIA NIH HHS AG34972NIA NIH HHS R01 AG015052NIA NIH HHS R01 AG034972NIA NIH HHS R37 AG015052
6 · The paper itself

Abstract

Factors secreted by the heart, referred to as "cardiokines," have diverse actions in the maintenance of cardiac homeostasis and remodeling. Follistatin-like 1 (Fstl1) is a secreted glycoprotein expressed in the adult heart and is induced in response to injurious conditions that promote myocardial hypertrophy and heart failure. The aim of this study was to investigate the role of cardiac Fstl1 in the remodeling response to pressure overload. Cardiac myocyte-specific Fstl1-KO mice were constructed and subjected to pressure overload induced by transverse aortic constriction (TAC). Although Fstl1-KO mice displayed no detectable baseline phenotype, TAC led to enhanced cardiac hypertrophic growth and a pronounced loss in ventricular performance by 4 wk compared with control mice. Conversely, mice that acutely or chronically overexpressed Fstl1 were resistant to pressure overload-induced hypertrophy and cardiac failure. Fstl1-deficient mice displayed a reduction in TAC-induced AMP-activated protein kinase (AMPK) activation in heart, whereas Fstl1 overexpression led to increased myocardial AMPK activation under these conditions. In cultured neonatal cardiomyocytes, administration of Fstl1 promoted AMPK activation and antagonized phenylephrine-induced hypertrophy. Inhibition of AMPK attenuated the antihypertrophic effect of Fstl1 treatment. These results document that cardiac Fstl1 functions as an autocrine/paracrine regulatory factor that antagonizes myocyte hypertrophic growth and the loss of ventricular performance in response to pressure overload, possibly through a mechanism involving the activation of the AMPK signaling axis.

Indexed as

Analysis of VarianceAnimalsBlotting, WesternCardiomegalyDNA PrimersEchocardiographyFollistatin-Related ProteinsMiceMice, KnockoutMyocytes, CardiacPressureReal-Time Polymerase Chain ReactionSignal TransductionStatistics, NonparametricVentricular RemodelingDNA PrimersFollistatin-Related ProteinsFstl1 protein, mouse

Identifiers

PMID21987816
PMCPMC3203781
OpenAlexW1988801254

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.