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Study · Animal study (in vivo) · mouse · 2020

2 results

Mitochondrial dysfunction in skeletal muscle of fukutin-deficient mice is resistant to exercise- and 5-aminoimidazole-4-carboxamide ribonucleotide-induced rescue.

Southern WM, Nichenko AS, Qualls AE, Portman K, Gidon A, Beedle AM, Call JA

Experimental physiology10 Sept 2020Cited by 7 (Europe PMC)

Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study2

2 results from studies that gave the peptide. No result from this study comes from people.

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In fukutin-deficient mice, AICAR failed to rescue mitochondrial deficits.

    In plain wordsIn fukutin-deficient mice, AICAR did not restore mitochondrial function compared with saline.

    Outcome
    No significant changeMitochondrial deficits
    Study

    mousen: not reported in source

    muscle-specific fukutin knockout mice
    Comparator
    saline
    Outcome group
    Mitochondrial function · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Treatment with the AMPK agonist 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) failed to rescue mitochondrial deficits in Fktn KO mice (P = 0.458)
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In healthy littermate and fukutin-deficient mice, AICAR improved recovery of muscle contractility after injury compared with saline.

    In plain wordsIn mice with and without fukutin deficiency, AICAR improved muscle contraction recovery after injury compared with saline.

    Outcome
    IncreaseRecovery of muscle contractility after injury
    Study

    mousen: not reported in source

    healthy littermate and muscle-specific fukutin knockout mice
    Comparator
    saline
    Outcome group
    Muscle injury and repair · Musculoskeletal
    Studied dose
    Dose not stated

    Measurements

    Improvement in contractility recovery
    ≈ 30%
    both LM and Fktn KO mice versus saline

    Source sentences

    Summary
    Treatment with the AMPK agonist 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) failed to rescue mitochondrial deficits in Fktn KO mice (P = 0.458) but did have beneficial (∼30% greater) effects on recovery of muscle contractility following injury in both LM and Fktn KO mice compared to saline…

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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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