Evidence map›Paper›PMID 21798096›Full record

ArticleSkeletal muscle2011

Role of TGF-β signaling in inherited and acquired myopathies.

Tyesha N Burks, Ronald D Cohn

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in Skeletal muscle, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05637216 (A Pilot Study of Losartan to Reduce Radiation Induced Fibrosis in Breast Cancer Patients), which is not on this map. Cited by 136 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
136citing papers in PubMed, 2 pooled it
5.5field-weighted citation impact, top 3% 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.

NCT05637216 phase2active not recruitingnot on this mapstarted 2023, after this paper: background citation

A Pilot Study of Losartan to Reduce Radiation Induced Fibrosis in Breast Cancer Patients

TypeinterventionalSponsorShaw Cancer CenterRan2023 to 2027Enrolled43ConditionsRadiation Induced FibrosisArmsLosartan 25 milligram capsule, Placebo
3 · Its place in the literature

Who cites it

136 citing papers in PubMed, 2 syntheses or guidelines pooled it, 223 citations in OpenAlex.

  1. Skeletal muscle alterations in Marfan syndrome: a systematic review.Journal of muscle research and cell motility · 2025
    Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Targeting TGF-β to Attenuate Ischemia-Reperfusion Associated Muscle Fibrosis and Enhance Regeneration: A Preclinical Study.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  6. Article
  7. Article
  8. Article
  9. Cancer cachexia: molecular basis and therapeutic advances.Signal transduction and targeted therapy · 2026
    Review
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  12. Article
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  14. Review
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  17. Review
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76 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

2 authors at 1 institution in 1 country.

Tyesha N BurksMcKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Ronald D Cohn
Johns Hopkins University · US

Funding

Predoctoral Training Program in Human GeneticsT32GM007814 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI VALLE, DAVID · 1985 to 2021
$10.6M
NIGMS NIH HHS T32 GM007814
6 · The paper itself

Abstract

The transforming growth factor-beta (TGF-β) superfamily consists of a variety of cytokines expressed in many different cell types including skeletal muscle. Members of this superfamily that are of particular importance in skeletal muscle are TGF-β1, mitogen-activated protein kinases (MAPKs), and myostatin. These signaling molecules play important roles in skeletal muscle homeostasis and in a variety of inherited and acquired neuromuscular disorders. Expression of these molecules is linked to normal processes in skeletal muscle such as growth, differentiation, regeneration, and stress response. However, chronic elevation of TGF-β1, MAPKs, and myostatin is linked to various features of muscle pathology, including impaired regeneration and atrophy. In this review, we focus on the aberrant signaling of TGF-β in various disorders such as Marfan syndrome, muscular dystrophies, sarcopenia, and critical illness myopathy. We also discuss how the inhibition of several members of the TGF-β signaling pathway has been implicated in ameliorating disease phenotypes, opening up novel therapeutic avenues for a large group of neuromuscular disorders.

Identifiers

PMID21798096
PMCPMC3156642
OpenAlexW2136938885

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.