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Study · Not a test of the peptide alone · 2021

1 result

Driving an Oxidative Phenotype Protects Myh4 Null Mice From Myofiber Loss During Postnatal Growth.

Zeng C, Shi H, Kirkpatrick LT, Ricome A, Park S, Scheffler JM, Hannon KM, Grant AL, Gerrard DE

Frontiers in physiology24 Feb 2022Cited by 6 (Europe PMC)

PMID35283757 (opens in a new tab)PMCIDPMC8908108 (opens in a new tab)DOI10.3389/fphys.2021.785151 (opens in a new tab)PepBankPUB-35283757
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Summary

Postnatal muscle growth is accompanied by increases in fast fiber type compositions and hypertrophy, raising the possibility that a slow to fast transition may be partially requisite for increases in muscle mass. To test this hypothesis, we ablated the Myh4 gene, and thus myosin heavy chain IIB protein and corresponding fibers in mice, and examined its consequences on postnatal muscle growth. Wild-type and Myh4 -/- mice had the same number of muscle fibers at 2 weeks postnatal. However, the gastrocnemius muscle lost up to 50% of its fibers between 2 and 4 weeks of age, though stabilizing thereafter. To compensate for the lack of functional IIB fibers, type I, IIA, and IIX(D) fibers increased in prevalence and size. To address whether slowing the slow-to-fast fiber transition process would rescue fiber loss in Myh4 -/- mice, we stimulated the oxidative program in muscle of Myh4 -/- mice either by overexpression of PGC-1α, a well-established model for fast-to-slow fiber transition, or by feeding mice AICAR, a potent AMP kinase agonist. Forcing an oxidative metabolism in muscle only partially protected the gastrocnemius muscle from loss of fibers in Myh4 -/- mice. To explore whether traditional means of stimulating muscle hypertrophy could overcome the muscling deficits in postnatal Myh4 -/- mice, myostatin null mice were bred with Myh4 -/- mice, or Myh4 -/- mice were fed the growth promotant clenbuterol. Interestingly, both genetic and pharmacological stimulations had little impact on mice lacking a functional Myh4 gene suggesting that the existing muscle fibers have maximized its capacity to enlarge to compensate for the lack of its neighboring IIB fibers. Curiously, however, cell signaling events responsible for IIB fiber formation remained intact in the tissue. These findings further show disrupting the slow-to-fast transition of muscle fibers compromises muscle growth postnatally and suggest that type IIB myosin heavy chain expression and its corresponding fiber type may be necessary for fiber maintenance, transition and hypertrophy in mice. The fact that forcing muscle metabolism toward a more oxidative phenotype can partially compensates for the lack of an intact Myh4 gene provides new avenues for attenuating the loss of fast-twitch fibers in aged or diseased muscles.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study1

No result from this study comes from a test of the peptide.

Studies that did not test the peptide alone1

In this study, AICAR (acadesine) was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking AICAR (acadesine).

  1. 01AnimalNot a test of AICAR (acadesine) aloneAnimal study (in vivo)Efficacy outcome

    In Myh4-null mice, oxidative metabolism induced with PGC-1α overexpression or AICAR only partially protected against gastrocnemius fiber loss.

    In plain wordsIn mice lacking Myh4, PGC-1α overexpression or AICAR only partly protected against muscle fiber loss.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseGastrocnemius fiber loss
    Study

    mousen: not reported in source

    Myh4-null mice
    Outcome group
    Muscle injury and repair · Musculoskeletal

    Source sentences

    Summary
    Forcing an oxidative metabolism in muscle only partially protected the gastrocnemius muscle from loss of fibers in Myh4 -/- mice.
    1 context sentence
    Summary · context
    To address whether slowing the slow-to-fast fiber transition process would rescue fiber loss in Myh4 -/- mice, we stimulated the oxidative program in muscle of Myh4 -/- mice either by overexpression of PGC-1α, a well-established model for fast-to-slow fiber transition, or by feeding mice AICAR, a potent AMP kinase agonist.

    In this study, AICAR (acadesine) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking AICAR (acadesine).

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    21 Oct 2026, 15:58 UTC

    Study results updated

  2. Version 1

    21 Oct 2026, 12:50 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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