Evidence map›Paper›PMID 21421824›Full record

ReviewAmerican journal of physiology. Heart and circulatory physiology2011

Myostatin from the heart: local and systemic actions in cardiac failure and muscle wasting.

Astrid Breitbart, Mannix Auger-Messier, Jeffery D Molkentin, Joerg Heineke

Abstract readReview
In one paragraph

Review in American journal of physiology. Heart and circulatory physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

70 citing papers in PubMed, 124 citations in OpenAlex.

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  16. Targeting MuRF1 to Combat Skeletal Muscle Wasting in Cardiac Cachexia: Mechanisms and Therapeutic Prospects.Medical science monitor : international medical journal of experimental and clinical research · 2024
    Review
  17. Exploring in vivo and in vitro models for heart failure with biomarker insights: a review.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2024
    Review
  18. Review
  19. Myostatin and the Heart.Biomolecules · 2023
    Review
  20. Review

10 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

4 authors at 3 institutions in 2 countries.

Astrid BreitbartMedizinische Hochschule Hannover, Klinik für Kardiologie und Angiologie, Rebirth-Cluster of Excellence, Carl-Neuberg-Str.1, 30625 Hannover, Germany.
Mannix Auger-Messier
Jeffery D Molkentin
Joerg Heineke
Medizinische Hochschule Hannover · DEHoward Hughes Medical Institute · USUniversity of Cincinnati · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A significant proportion of heart failure patients develop skeletal muscle wasting and cardiac cachexia, which is associated with a very poor prognosis. Recently, myostatin, a cytokine from the transforming growth factor-β (TGF-β) family and a known strong inhibitor of skeletal muscle growth, has been identified as a direct mediator of skeletal muscle atrophy in mice with heart failure. Myostatin is mainly expressed in skeletal muscle, although basal expression is also detectable in heart and adipose tissue. During pathological loading of the heart, the myocardium produces and secretes myostatin into the circulation where it inhibits skeletal muscle growth. Thus, genetic elimination of myostatin from the heart reduces skeletal muscle atrophy in mice with heart failure, whereas transgenic overexpression of myostatin in the heart is capable of inducing muscle wasting. In addition to its endocrine action on skeletal muscle, cardiac myostatin production also modestly inhibits cardiomyocyte growth under certain circumstances, as well as induces cardiac fibrosis and alterations in ventricular function. Interestingly, heart failure patients show elevated myostatin levels in their serum. To therapeutically influence skeletal muscle wasting, direct inhibition of myostatin was shown to positively impact skeletal muscle mass in heart failure, suggesting a promising strategy for the treatment of cardiac cachexia in the future.

Indexed as

AnimalsCachexiaDisease Models, AnimalHeart FailureHumansMiceMice, TransgenicMuscle, SkeletalMuscular AtrophyMyocardiumMyostatinMyostatin

Identifiers

PMID21421824
PMCPMC3119101
OpenAlexW2168867523

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.