Evidence map›Paper›PMID 32310830›Full record

ArticleJCI insight2020

Myocyte-derived Myomaker expression is required for regenerative fusion but exacerbates membrane instability in dystrophic myofibers.

Michael J Petrany, Taejeong Song, Sakthivel Sadayappan, Douglas P Millay

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

28 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Myomaker and Myomixer are required for craniofacial myoblast fusion in zebrafish.Developmental dynamics : an official publication of the American Association of Anatomists · 2026
    Article
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  9. Review
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  11. Molecular regulation of myocyte fusion.Current topics in developmental biology · 2024
    Review
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  18. All for One and One for All: Regenerating Skeletal Muscle.Cold Spring Harbor perspectives in biology · 2022
    Review
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

Michael J PetranyDivision of Molecular Cardiovascular Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.
Taejeong SongDepartment of Internal Medicine, Division of Cardiovascular Health and Disease, and.
Sakthivel SadayappanDepartment of Internal Medicine, Division of Cardiovascular Health and Disease, and.
Douglas P MillayDivision of Molecular Cardiovascular Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.
Cincinnati Children's Hospital Medical Center · US

Funding

Medical Scientist Training ProgramT32GM063483 · NIGMS · UNIVERSITY OF CINCINNATI · PI KHURANA HERSHEY, GURJIT K. · 2002 to 2022
$6.7M
Pulmonary Development and Disease Pathogenesis Training ProgramT32HL007752 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI Francis Xavier McCormack, Anne-Karina Theresia Perl · 1994 to 2026
$6.3M
Fast myosin binding protein-C and cardiac contractility in heart failureR01HL105826 · NHLBI · UNIVERSITY OF CINCINNATI · PI SADAYAPPAN, SAKTHIVEL · 2011 to 2025
$4.5M
Deciphering mechanisms of myoblast fusionR01AR068286 · NIAMS · CINCINNATI CHILDRENS HOSP MED CTR · PI MILLAY, DOUGLAS PAUL · 2015 to 2024
$4.2M
Skeletal Myosin-Binding Protein C (MyBP-C): Molecular Structure and FunctionR01AR067279 · NIAMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CRAIG, ROGER W, WARSHAW, DAVID M · 2015 to 2019
$2.3M
Role of skeletal muscle stem cell fusion and fibrosis during agingR01AG059605 · NIA · CINCINNATI CHILDRENS HOSP MED CTR · PI MILLAY, DOUGLAS PAUL · 2018 to 2022
$1.7M
IGF-2R is a new therapeutic target for cardiac ischemia-reperfusion injuryR01HL143490 · NHLBI · UNIVERSITY OF CINCINNATI · PI WANG, YIGANG · 2019 to 2022
$1.6M
Molecular mechanism of hypertrophic cardiomyopathy in populations of South Asian descendantsR01HL130356 · NHLBI · UNIVERSITY OF CINCINNATI · PI SADAYAPPAN, SAKTHIVEL · 2016 to 2019
$1.6M
Myoarchitectural Basis of Heart FailureR56HL139680 · NHLBI · OCEAN STATE RESEARCH INSTITUTE, INC. · PI GILBERT, RICHARD J · 2018 to 2018
$431k
Integrative Approaches to Complex Cardiovascular DiseasesR13HL149313 · NHLBI · STANFORD UNIVERSITY · PI SADAYAPPAN, SAKTHIVEL, TARDIFF, JIL C · 2019 to 2019
$30k
NHLBI NIH HHS R01 HL105826NHLBI NIH HHS R01 HL130356NHLBI NIH HHS R01 HL143490NHLBI NIH HHS R13 HL149313NHLBI NIH HHS R56 HL139680NHLBI NIH HHS T32 HL007752NIAMS NIH HHS R01 AR067279NIAMS NIH HHS R01 AR068286NIA NIH HHS R01 AG059605NIGMS NIH HHS T32 GM063483
6 · The paper itself

Abstract

Muscle progenitor cell fusion is required for the formation and regeneration of multinucleated skeletal muscle fibers. Chronic muscle regeneration in Duchenne muscular dystrophy (DMD) is characterized by ongoing fusion of satellite cell (SC) progeny, but the effects of fusion on disease and the mechanisms by which fusion is accomplished in this setting are not fully understood. Using the mdx mouse model of DMD, we deleted the fusogenic protein Myomaker in SCs or myofibers. Following deletion in SCs, mice displayed a complete lack of myocyte fusion, resulting in severe muscle loss, enhanced fibrosis, and significant functional decline. Reduction of Myomaker in mature myofibers in mdx mice, however, led to minimal alterations in fusion dynamics. Unexpectedly, myofiber-specific deletion of Myomaker resulted in improvement of disease phenotype, with enhanced function and decreased muscle damage. Our data indicate that Myomaker has divergent effects on dystrophic disease severity depending upon its compartment of expression. These findings show that myocyte fusion is absolutely required for effective regeneration in DMD, but persistent Myomaker expression in myofibers due to ongoing fusion may have unintended deleterious consequences for muscle integrity. Thus, sustained activation of a component of the myogenic program in dystrophic myofibers exacerbates disease.

Indexed as

Muscle Fibers, SkeletalRegenerationAnimalsCell FusionMembrane ProteinsMiceMice, Inbred mdxMice, KnockoutMuscle DevelopmentMuscle ProteinsMuscular Dystrophy, DuchenneMembrane ProteinsMuscle ProteinsMymk protein, mouseMuscle BiologySkeletal muscleStem cells

Identifiers

PMID32310830
PMCPMC7253022
OpenAlexW3016304962

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.