Evidence map›Paper›PMID 26798450›Full record

ArticleSkeletal muscle2016

Decrease of myofiber branching via muscle-specific expression of the olfactory receptor mOR23 in dystrophic muscle leads to protection against mechanical stress.

Christophe Pichavant, Thomas J Burkholder, Grace K Pavlath

Open access · goldAbstract read
In one paragraph

Article in Skeletal muscle, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

20 citing papers in PubMed, 32 citations in OpenAlex.

  1. Twisting Paths: The Paradox of Fiber Branching in Muscle Regeneration.International journal of molecular sciences · 2026
    Review
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  11. Lifespan Analysis of DystrophicFrontiers in physiology · 2021
    Article
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  14. Comprehensive evaluation of the metabolic effects of insect meal fromJournal of animal science and biotechnology · 2020
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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

3 authors at 2 institutions in 1 country.

Christophe PichavantDepartment of Pharmacology, Emory University, Atlanta, GA USA ; Present address: Department of Genetics, Stanford University, Stanford, CA USA.
Thomas J BurkholderSchool of Applied Physiology, Georgia Institute of Technology, Atlanta, GA USA.
Grace K PavlathDepartment of Pharmacology, Emory University, Atlanta, GA USA ; 1510 Clifton Road, Room 5024, Atlanta, GA 30322 USA.
Emory University · USGeorgia Institute of Technology · US

Funding

Olfactory receptor signaling in skeletal muscleR01AR061267 · NIAMS · EMORY UNIVERSITY · PI PAVLATH, GRACE K · 2012 to 2016
$1.7M
NIAMS NIH HHS AR061267NIAMS NIH HHS R01 AR061267
6 · The paper itself

Abstract

backgroundAbnormal branched myofibers within skeletal muscles are commonly found in diverse animal models of muscular dystrophy as well as in patients. Branched myofibers from dystrophic mice are more susceptible to break than unbranched myofibers suggesting that muscles containing a high percentage of these myofibers are more prone to injury. Previous studies showed ubiquitous over-expression of mouse olfactory receptor 23 (mOR23), a G protein-coupled receptor, in wild type mice decreased myofiber branching. Whether mOR23 over-expression specifically in skeletal muscle cells is sufficient to mitigate myofiber branching in dystrophic muscle is unknown.

methodsWe created a novel transgenic mouse over-expressing mOR23 specifically in muscle cells and then bred with dystrophic (mdx) mice. Myofiber branching was analyzed in these two transgenic mice and membrane integrity was assessed by Evans blue dye fluorescence.

resultsmOR23 over-expression in muscle led to a decrease of myofiber branching after muscle regeneration in non-dystrophic mouse muscles and reduced the severity of myofiber branching in mdx mouse muscles. Muscles from mdx mouse over-expressing mOR23 significantly exhibited less damage to eccentric contractions than control mdx muscles.

conclusionsThe decrease of myofiber branching in mdx mouse muscles over-expressing mOR23 reduced the amount of membrane damage induced by mechanical stress. These results suggest that modifying myofiber branching in dystrophic patients, while not preventing degeneration, could be beneficial for mitigating some of the effects of the disease process.

Indexed as

Muscle ContractionAge FactorsAnimalsBarium CompoundsCell MembraneChloridesDisease Models, AnimalFemaleHybridization, GeneticMaleMice, Inbred mdxMice, TransgenicMuscle, SkeletalMuscular Dystrophy, DuchenneMyofibrilsReceptors, Odorantbarium chlorideBarium CompoundsChloridesOlfr16 protein, mouseReceptors, OdorantMechanical stressmOR23Muscle regenerationMuscular dystrophyMyofiber branching

Identifiers

PMID26798450
PMCPMC4721043
OpenAlexW2256959533

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.