Evidence map›Paper›PMID 25591711›Full record

ArticleJournal of translational medicine2015

Myostatin and IGF-I signaling in end-stage human heart failure: a qRT-PCR study.

Júlia Aliz Baán, Zoltán V Varga, Przemyslaw Leszek, Mariusz Kuśmierczyk, Tamás Baranyai, László Dux, Péter Ferdinandy, Thomas Braun, Luca Mendler

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
7.4field-weighted citation impact, top 2% 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, 1 synthesis or guideline pooled it, 139 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Myostatin and the Heart.Biomolecules · 2023
    Review
  5. Smad3 promotes adverse cardiovascular remodeling and dysfunction in doxorubicin-treated hearts.American journal of physiology. Heart and circulatory physiology · 2022
    Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Considerations for anFrontiers in pharmacology · 2019
    Review
  13. Review
  14. Article
  15. The TGF-β pathway mediates doxorubicin effects on cardiac endothelial cells.Journal of molecular and cellular cardiology · 2016
    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 5 institutions in 3 countries.

Júlia Aliz Baán
Zoltán V Varga
Przemyslaw Leszek
Mariusz Kuśmierczyk
Tamás Baranyai
László Dux
Péter Ferdinandy
Thomas Braun
Luca Mendler
Semmelweis University · HUInstitute of Cardiology · PLUniversity of Szeged · HUGoethe University Frankfurt · DEMax Planck Institute for Heart and Lung Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMyostatin (Mstn) is a key regulator of heart metabolism and cardiomyocyte growth interacting tightly with insulin-like growth factor I (IGF-I) under physiological conditions. The pathological role of Mstn has also been suggested since Mstn protein was shown to be upregulated in the myocardium of end-stage heart failure. However, no data are available about the regulation of gene expression of Mstn and IGF-I in different regions of healthy or pathologic human hearts, although they both might play a crucial role in the pathomechanism of heart failure.

methodsIn the present study, heart samples were collected from left ventricles, septum and right ventricles of control healthy individuals as well as from failing hearts of dilated (DCM) or ischemic cardiomyopathic (ICM) patients. A comprehensive qRT-PCR analysis of Mstn and IGF-I signaling was carried out by measuring expression of Mstn, its receptor Activin receptor IIB (ActRIIB), IGF-I, IGF-I receptor (IGF-IR), and the negative regulator of Mstn miR-208, respectively. Moreover, we combined the measured transcript levels and created complex parameters characterizing either Mstn- or IGF-I signaling in the different regions of healthy or failing hearts.

resultsWe have found that in healthy control hearts, the ratio of Mstn/IGF-I signaling was significantly higher in the left ventricle/septum than in the right ventricle. Moreover, Mstn transcript levels were significantly upregulated in all heart regions of DCM but not ICM patients. However, the ratio of Mstn/IGF-I signaling remained increased in the left ventricle/septum compared to the right ventricle of DCM patients (similarly to the healthy hearts). In contrast, in ICM hearts significant transcript changes were detected mainly in IGF-I signaling. In parallel with these results miR-208 showed mild upregulation in the left ventricle of both DCM and ICM hearts.

conclusionsThis is the first demonstration of a spatial asymmetry in the expression pattern of Mstn/IGF-I in healthy hearts, which is likely to play a role in the different growth regulation of left vs. right ventricle. Moreover, we identified Mstn as a massively regulated gene in DCM but not in ICM as part of possible compensatory mechanisms in the failing heart.

Indexed as

Signal TransductionAdultAgedBase SequenceCase-Control StudiesDNA PrimersFemaleHeart FailureHumansInsulin-Like Growth Factor IMaleMiddle AgedMyostatinPolymerase Chain ReactionDNA PrimersInsulin-Like Growth Factor IMyostatin

Identifiers

PMID25591711
PMCPMC4301667
OpenAlexW2131437431

What OpenQuestion holds

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LicenceCC BY
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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.