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Study · Animal study (in vivo) · mouse · 2016

5 results

Sustained AMPK activation improves muscle function in a mitochondrial myopathy mouse model by promoting muscle fiber regeneration.

Peralta S, Garcia S, Yin HY, Arguello T, Diaz F, Moraes CT

Human molecular genetics10 Jun 2016Cited by 28 (Europe PMC)

PMID27288451 (opens in a new tab)PMCIDPMC5179920 (opens in a new tab)DOI10.1093/hmg/ddw167 (opens in a new tab)PepBankPUB-27288451
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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 study5

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In mitochondrial myopathy mice, prolonged AICAR treatment improved cytochrome c oxidase activity.

    In plain wordsIn mice with mitochondrial muscle disease, AICAR improved cytochrome c oxidase activity.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseCytochrome c oxidase activity
    Study

    mousen: not reported in source

    Cox10-Mef2c-Cre mitochondrial myopathy
    Outcome group
    Mitochondrial function · Musculoskeletal
    Studied dose
    Dose not stated · 3 monthsAs given in this study (mouse).

    Source sentences

    Summary
    We treated the animals for 3 months and found that sustained AMP-dependent kinase activation improved cytochrome c oxidase activity, rescued the motor phenotype and delayed the onset of the myopathy.
    1 context sentence
    Summary · context
    We asked whether prolonged AICAR treatment is beneficial in a mouse model of slowly progressing mitochondrial myopathy (Cox10-Mef2c-Cre), and whether the compensatory mechanism is indeed an increase in mitochondrial biogenesis.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In mitochondrial myopathy mice, AICAR rescued motor function, whether treatment began before or after disease onset.

    In plain wordsIn mice, AICAR improved movement when treatment began before or after muscle disease appeared.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseMotor phenotype
    Study

    mousen: not reported in source

    Cox10-Mef2c-Cre mitochondrial myopathy
    Outcome group
    Exercise and physical function · Musculoskeletal
    Studied dose
    Dose not stated · 3 monthsAs given in this study (mouse).

    Source sentences

    Summary
    We treated the animals for 3 months and found that sustained AMP-dependent kinase activation improved cytochrome c oxidase activity, rescued the motor phenotype and delayed the onset of the myopathy.
    2 context sentences
    Summary · context
    This improvement was observed whether treatment started before or after the onset of the disease.
    Summary · context
    We asked whether prolonged AICAR treatment is beneficial in a mouse model of slowly progressing mitochondrial myopathy (Cox10-Mef2c-Cre), and whether the compensatory mechanism is indeed an increase in mitochondrial biogenesis.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In mitochondrial myopathy mice, prolonged AICAR treatment delayed myopathy onset.

    In plain wordsIn mice, AICAR delayed the onset of mitochondrial muscle disease.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseMyopathy onset
    Study

    mousen: not reported in source

    Cox10-Mef2c-Cre mitochondrial myopathy
    Outcome group
    Muscle injury and repair · Musculoskeletal
    Studied dose
    Dose not stated · 3 monthsAs given in this study (mouse).

    Source sentences

    Summary
    We treated the animals for 3 months and found that sustained AMP-dependent kinase activation improved cytochrome c oxidase activity, rescued the motor phenotype and delayed the onset of the myopathy.
    1 context sentence
    Summary · context
    We asked whether prolonged AICAR treatment is beneficial in a mouse model of slowly progressing mitochondrial myopathy (Cox10-Mef2c-Cre), and whether the compensatory mechanism is indeed an increase in mitochondrial biogenesis.
  4. 04AnimalAnimal study (in vivo)Efficacy outcome

    In mitochondrial myopathy mice, AICAR increased skeletal muscle regeneration.

    In plain wordsIn mice, AICAR increased skeletal muscle regeneration.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseSkeletal muscle regeneration
    Study

    mousen: not reported in source

    Cox10-Mef2c-Cre mitochondrial myopathy
    Outcome group
    Muscle injury and repair · Musculoskeletal
    Studied dose
    Dose not stated · 3 monthsAs given in this study (mouse).

    Source sentences

    Summary
    We found that AICAR increased skeletal muscle regeneration thereby decreasing the levels of deleted Cox10-floxed alleles.
    1 context sentence
    Summary · context
    We asked whether prolonged AICAR treatment is beneficial in a mouse model of slowly progressing mitochondrial myopathy (Cox10-Mef2c-Cre), and whether the compensatory mechanism is indeed an increase in mitochondrial biogenesis.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In mitochondrial myopathy mice, AICAR-associated muscle regeneration reduced deleted Cox10-floxed allele levels.

    In plain wordsIn mice, AICAR-related muscle regeneration reduced deleted Cox10-floxed allele levels.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseDeleted Cox10-floxed alleles
    Study

    mousen: not reported in source

    Cox10-Mef2c-Cre mitochondrial myopathy
    Outcome group
    Receptor activity and mechanism · Musculoskeletal
    Studied dose
    Dose not stated · 3 monthsAs given in this study (mouse).

    Source sentences

    Summary
    We found that AICAR increased skeletal muscle regeneration thereby decreasing the levels of deleted Cox10-floxed alleles.
    1 context sentence
    Summary · context
    We asked whether prolonged AICAR treatment is beneficial in a mouse model of slowly progressing mitochondrial myopathy (Cox10-Mef2c-Cre), and whether the compensatory mechanism is indeed an increase in mitochondrial biogenesis.

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

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