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Study · Animal study (in vivo) · mouse · 2012

7 results

AMPK activation stimulates autophagy and ameliorates muscular dystrophy in the mdx mouse diaphragm.

Pauly M, Daussin F, Burelle Y, Li T, Godin R, Fauconnier J, Koechlin-Ramonatxo C, Hugon G, Lacampagne A, Coisy-Quivy M, Liang F, Hussain S, Matecki S, Petrof BJ

The American journal of pathology5 Jun 2012Cited by 184 (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 study7

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

  1. 01AnimalAnimal study (in vivo)Mechanism

    In mdx mice, AICAR triggered diaphragm autophagy.

    In plain wordsIn mice with muscular dystrophy, AICAR increased diaphragm autophagy.

    Outcome
    IncreaseAutophagy
    Study

    mousen: not reported in source

    mdx mouse diaphragm
    Outcome group
    Muscle injury and repair · Musculoskeletal
    Studied dose
    Dose not stated · 4 weeksAs given in this study (mouse).

    Source sentences

    Summary
    Treatment of mdx mice for 4 weeks with an established AMPK agonist, AICAR (5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside), potently triggered autophagy in the mdx diaphragm without inducing muscle fiber atrophy.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In mdx mice, AICAR triggered autophagy without inducing muscle fiber atrophy.

    In plain wordsIn mice with muscular dystrophy, AICAR did not induce muscle fiber atrophy.

    Outcome
    Direction not reportedMuscle fiber atrophy
    Study

    mousen: not reported in source

    mdx mouse diaphragm
    Outcome group
    Muscle injury and repair · Musculoskeletal
    Studied dose
    Dose not stated · 4 weeksAs given in this study (mouse).

    Source sentences

    Summary
    Treatment of mdx mice for 4 weeks with an established AMPK agonist, AICAR (5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside), potently triggered autophagy in the mdx diaphragm without inducing muscle fiber atrophy.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In mdx mice, AICAR normalized exaggerated diaphragm mitochondrial sensitivity to calcium-induced permeability transition pore opening.

    In plain wordsIn mice with muscular dystrophy, AICAR normalized excessive sensitivity of diaphragm mitochondria to calcium-induced pore opening.

    Outcome
    DecreaseCalcium-induced permeability transition sensitivity
    Study

    mousen: not reported in source

    mdx mouse diaphragm
    Outcome group
    Mitochondrial function · Musculoskeletal
    Studied dose
    Dose not stated · 4 weeksAs given in this study (mouse).

    Source sentences

    Summary
    In AICAR-treated mdx mice, the exaggerated sensitivity of mdx diaphragm mitochondria to calcium-induced permeability transition pore opening was restored to normal levels.
    1 context sentence
    Summary · context
    Treatment of mdx mice for 4 weeks with an established AMPK agonist, AICAR (5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside), potently triggered autophagy in the mdx diaphragm without inducing muscle fiber atrophy.
  4. 04AnimalAnimal study (in vivo)Efficacy outcome

    In mdx mice, AICAR treatment was associated with improved diaphragm histopathology.

    In plain wordsIn mice with muscular dystrophy, AICAR treatment was associated with improved diaphragm tissue structure.

    Outcome
    Direction not reportedDiaphragm histopathology
    Study

    mousen: not reported in source

    mdx mouse diaphragm
    Outcome group
    Muscle injury and repair · Musculoskeletal
    Studied dose
    Dose not stated · 4 weeksAs given in this study (mouse).

    Source sentences

    Summary
    There were associated improvements in mdx diaphragm histopathology and in maximal force-generating capacity, which were not linked to increased mitochondrial biogenesis or up-regulated utrophin expression.
    1 context sentence
    Summary · context
    Treatment of mdx mice for 4 weeks with an established AMPK agonist, AICAR (5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside), potently triggered autophagy in the mdx diaphragm without inducing muscle fiber atrophy.
  5. 05AnimalAnimal study (in vivo)Efficacy outcome

    In mdx mice, AICAR treatment was associated with improved maximal diaphragm force-generating capacity.

    In plain wordsIn mice with muscular dystrophy, AICAR treatment was associated with greater maximal diaphragm force.

    Outcome
    IncreaseMaximal force-generating capacity
    Study

    mousen: not reported in source

    mdx mouse diaphragm
    Outcome group
    Exercise and physical function · Musculoskeletal
    Studied dose
    Dose not stated · 4 weeksAs given in this study (mouse).

    Source sentences

    Summary
    There were associated improvements in mdx diaphragm histopathology and in maximal force-generating capacity, which were not linked to increased mitochondrial biogenesis or up-regulated utrophin expression.
    1 context sentence
    Summary · context
    Treatment of mdx mice for 4 weeks with an established AMPK agonist, AICAR (5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside), potently triggered autophagy in the mdx diaphragm without inducing muscle fiber atrophy.
  6. 06AnimalAnimal study (in vivo)Mechanism

    In mdx mice, diaphragm improvements after AICAR were not linked to increased mitochondrial biogenesis.

    In plain wordsIn mice with muscular dystrophy, diaphragm improvements after AICAR were not linked to increased mitochondrial biogenesis.

    Outcome
    Not applicableMitochondrial biogenesis linkage
    Study

    mousen: not reported in source

    mdx mouse diaphragm
    Outcome group
    Mitochondrial function · Musculoskeletal
    Studied dose
    Dose not stated · 4 weeksAs given in this study (mouse).

    Source sentences

    Summary
    There were associated improvements in mdx diaphragm histopathology and in maximal force-generating capacity, which were not linked to increased mitochondrial biogenesis or up-regulated utrophin expression.
    1 context sentence
    Summary · context
    Treatment of mdx mice for 4 weeks with an established AMPK agonist, AICAR (5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside), potently triggered autophagy in the mdx diaphragm without inducing muscle fiber atrophy.
  7. 07AnimalAnimal study (in vivo)Mechanism

    In mdx mice, diaphragm improvements after AICAR were not linked to up-regulated utrophin expression.

    In plain wordsIn mice with muscular dystrophy, diaphragm improvements after AICAR were not linked to increased utrophin expression.

    Outcome
    Not applicableUtrophin expression linkage
    Study

    mousen: not reported in source

    mdx mouse diaphragm
    Outcome group
    Muscle injury and repair · Musculoskeletal
    Studied dose
    Dose not stated · 4 weeksAs given in this study (mouse).

    Source sentences

    Summary
    There were associated improvements in mdx diaphragm histopathology and in maximal force-generating capacity, which were not linked to increased mitochondrial biogenesis or up-regulated utrophin expression.
    1 context sentence
    Summary · context
    Treatment of mdx mice for 4 weeks with an established AMPK agonist, AICAR (5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside), potently triggered autophagy in the mdx diaphragm without inducing muscle fiber atrophy.

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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