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Study · Animal study (in vivo) · mouse · 2018

4 results

Pharmacological and physiological activation of AMPK improves the spliceopathy in DM1 mouse muscles.

Ravel-Chapuis A, Al-Rewashdy A, Bélanger G, Jasmin BJ

Human molecular genetics1 Oct 2018Cited by 33 (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 study4

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In DM1 mice, AICAR promoted a slower, more oxidative muscle phenotype.

    In plain wordsIn mice with myotonic dystrophy, AICAR promoted a slower, more oxidative muscle phenotype.

    Outcome
    IncreaseSlower oxidative muscle phenotype
    Study

    mousen: not reported in source

    HSALR myotonic dystrophy type 1 mice
    Outcome group
    Muscle injury and repair · Musculoskeletal
    Studied dose
    Dose not stated · 6 weeksAs given in this study (mouse).

    Source sentences

    Summary
    Indeed, a 6-week AICAR treatment of DM1 mice promoted expression of a slower, more oxidative phenotype, improved muscle histology and corrected several events associated with RNA toxicity.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In DM1 mice, AICAR improved muscle histology.

    In plain wordsIn mice with myotonic dystrophy, AICAR improved muscle tissue structure.

    Outcome
    IncreaseMuscle histology
    Study

    mousen: not reported in source

    HSALR myotonic dystrophy type 1 mice
    Outcome group
    Muscle injury and repair · Musculoskeletal
    Studied dose
    Dose not stated · 6 weeksAs given in this study (mouse).

    Source sentences

    Summary
    Indeed, a 6-week AICAR treatment of DM1 mice promoted expression of a slower, more oxidative phenotype, improved muscle histology and corrected several events associated with RNA toxicity.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In DM1 mice, AICAR corrected several events associated with RNA toxicity.

    In plain wordsIn mice with myotonic dystrophy, AICAR corrected several events linked to RNA toxicity.

    Outcome
    DecreaseRNA toxicity-associated events
    Study

    mousen: not reported in source

    HSALR myotonic dystrophy type 1 mice
    Outcome group
    Muscle injury and repair · Musculoskeletal
    Studied dose
    Dose not stated · 6 weeksAs given in this study (mouse).

    Source sentences

    Summary
    Indeed, a 6-week AICAR treatment of DM1 mice promoted expression of a slower, more oxidative phenotype, improved muscle histology and corrected several events associated with RNA toxicity.
  4. 04LabIn vitro (cells)Efficacy outcome

    In patient-derived DM1 myoblasts, AICAR improved spliceopathy in a dose-dependent manner.

    In plain wordsIn lab tests with DM1 muscle cells, AICAR improved RNA splicing defects in a dose-dependent manner.

    Outcome
    DecreaseSpliceopathy
    Study

    humann: not reported in source

    Patient-derived DM1 myoblasts
    Outcome group
    Muscle injury and repair · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Importantly, AICAR also had a dose-dependent positive effect on the spliceopathy in patient-derived DM1 myoblasts.

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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