Evidence map›Paper›PMID 20887891›Full record

ArticleCell2010

Myogenin and class II HDACs control neurogenic muscle atrophy by inducing E3 ubiquitin ligases.

Viviana Moresi, Andrew H Williams, Eric Meadows, Jesse M Flynn, Matthew J Potthoff, John McAnally, John M Shelton, Johannes Backs, William H Klein, James A Richardson and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 270 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
270citing papers in PubMed, 2 pooled it
9.2field-weighted citation impact, top 1% 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

270 citing papers in PubMed, 2 syntheses or guidelines pooled it, 447 citations in OpenAlex.

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  14. The multimodal transcriptional response of denervated skeletal muscle involves regulation ofProceedings of the National Academy of Sciences of the United States of America · 2025
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210 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 2 institutions in 1 country.

Viviana MoresiDepartment of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Andrew H Williams
Eric Meadows
Jesse M Flynn
Matthew J Potthoff
John McAnally
John M Shelton
Johannes Backs
William H Klein
James A Richardson
Rhonda Bassel-Duby
Eric N Olson
The University of Texas Southwestern Medical Center · USThe University of Texas MD Anderson Cancer Center · US

Funding

Heart Repair through Reprogramming of Cardiac Cell FateR01HL077439 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI OLSON, ERIC N · 2004 to 2015
$6.2M
TRANSCRIPTIONAL CONTROL OF CARDIAC MUSCLE DEVELOPMENTR37HL053351 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI OLSON, ERIC N · 2000 to 2009
$3.7M
MicroRNA Control of Cardiac Gene Expression, Function and DiseaseR01HL093039 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI OLSON, ERIC N · 2009 to 2013
$2.8M
NHLBI NIH HHS R01 HL077439NHLBI NIH HHS R01 HL093039NHLBI NIH HHS R37 HL053351
6 · The paper itself

Abstract

Maintenance of skeletal muscle structure and function requires innervation by motor neurons, such that denervation causes muscle atrophy. We show that myogenin, an essential regulator of muscle development, controls neurogenic atrophy. Myogenin is upregulated in skeletal muscle following denervation and regulates expression of the E3 ubiquitin ligases MuRF1 and atrogin-1, which promote muscle proteolysis and atrophy. Deletion of myogenin from adult mice diminishes expression of MuRF1 and atrogin-1 in denervated muscle and confers resistance to atrophy. Mice lacking histone deacetylases (HDACs) 4 and 5 in skeletal muscle fail to upregulate myogenin and also preserve muscle mass following denervation. Conversely, forced expression of myogenin in skeletal muscle of HDAC mutant mice restores muscle atrophy following denervation. Thus, myogenin plays a dual role as both a regulator of muscle development and an inducer of neurogenic atrophy. These findings reveal a specific pathway for muscle wasting and potential therapeutic targets for this disorder.

Indexed as

AnimalsAtrophyHistone DeacetylasesMiceMice, KnockoutMuscle ProteinsMuscle, SkeletalMyogeninSKP Cullin F-Box Protein LigasesTripartite Motif ProteinsUbiquitin-Protein LigasesFbxo32 protein, mouseHdac5 protein, mouseHistone DeacetylasesMuscle ProteinsMyogeninSKP Cullin F-Box Protein LigasesTrim63 protein, mouseTripartite Motif ProteinsUbiquitin-Protein Ligases

Identifiers

PMID20887891
PMCPMC2982779
OpenAlexW2162063376

What OpenQuestion holds

Textmetadata
LicenceTDM
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.