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

7 results

Chronic AMPK stimulation attenuates adaptive signaling in dystrophic skeletal muscle.

Ljubicic V, Khogali S, Renaud JM, Jasmin BJ

American journal of physiology. Cell physiology21 Sept 2011Cited by 52 (Europe PMC)

PMID21940670 (opens in a new tab)DOI10.1152/ajpcell.00183.2011 (opens in a new tab)PepBankPUB-21940670
Publisher pagePubMedAsk about this study
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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 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, chronic AICAR attenuated running-elicited AMPK phosphorylation versus vehicle.

    In plain wordsIn mice with muscular dystrophy, AICAR reduced running-elicited AMPK phosphorylation versus vehicle.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseRunning-elicited AMPK phosphorylation
    Study

    mousen: not reported in source

    mdx dystrophic skeletal muscle
    Comparator
    Vehicle-treated mice
    Outcome group
    Receptor activity and mechanism · Musculoskeletal
    Studied dose
    500 mg·kg(-1)·day(-1) · 30 daysAs given in this study (mouse).

    Source sentences

    Summary
    In the mdx animals that received the chronic AICAR treatment, running-elicited AMPK and p38 phosphorylation was attenuated compared with vehicle-treated mice.
    1 context sentence
    Summary · context
    mdx mice were treated with the AMP-activated protein kinase (AMPK) activator 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside (AICAR; 500 mg·kg(-1)·day(-1)) for 30 days, and then one-half of the animals were subjected to a bout of treadmill running to induce acute AMPK and p38 MAPK signaling.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In mdx mice, chronic AICAR attenuated running-elicited p38 phosphorylation versus vehicle.

    In plain wordsIn mice with muscular dystrophy, AICAR reduced running-elicited p38 phosphorylation versus vehicle.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseRunning-elicited p38 phosphorylation
    Study

    mousen: not reported in source

    mdx dystrophic skeletal muscle
    Comparator
    Vehicle-treated mice
    Outcome group
    Receptor activity and mechanism · Musculoskeletal
    Studied dose
    500 mg·kg(-1)·day(-1) · 30 daysAs given in this study (mouse).

    Source sentences

    Summary
    In the mdx animals that received the chronic AICAR treatment, running-elicited AMPK and p38 phosphorylation was attenuated compared with vehicle-treated mice.
    1 context sentence
    Summary · context
    mdx mice were treated with the AMP-activated protein kinase (AMPK) activator 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside (AICAR; 500 mg·kg(-1)·day(-1)) for 30 days, and then one-half of the animals were subjected to a bout of treadmill running to induce acute AMPK and p38 MAPK signaling.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In mdx mice, chronic AICAR blunted stress-evoked PPARδ expression compared with vehicle-treated mice.

    In plain wordsIn mice with muscular dystrophy, chronic AICAR blunted stress-evoked PPARδ expression versus vehicle.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreasePPARδ expression
    Study

    mousen: not reported in source

    mdx dystrophic skeletal muscle
    Comparator
    Vehicle-treated mice
    Outcome group
    Receptor activity and mechanism · Musculoskeletal
    Studied dose
    500 mg·kg(-1)·day(-1) · 30 daysAs given in this study (mouse).

    Source sentences

    Summary
    Similarly, acute stress-evoked expression of PPARδ, PGC-1α, and SIRT1 was also blunted by chronic pharmacological AMPK stimulation.
    1 context sentence
    Summary · context
    mdx mice were treated with the AMP-activated protein kinase (AMPK) activator 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside (AICAR; 500 mg·kg(-1)·day(-1)) for 30 days, and then one-half of the animals were subjected to a bout of treadmill running to induce acute AMPK and p38 MAPK signaling.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In mdx mice, chronic AICAR blunted stress-evoked PGC-1α expression compared with vehicle-treated mice.

    In plain wordsIn mice with muscular dystrophy, chronic AICAR blunted stress-evoked PGC-1α expression versus vehicle.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreasePGC-1α expression
    Study

    mousen: not reported in source

    mdx dystrophic skeletal muscle
    Comparator
    Vehicle-treated mice
    Outcome group
    Receptor activity and mechanism · Musculoskeletal
    Studied dose
    500 mg·kg(-1)·day(-1) · 30 daysAs given in this study (mouse).

    Source sentences

    Summary
    Similarly, acute stress-evoked expression of PPARδ, PGC-1α, and SIRT1 was also blunted by chronic pharmacological AMPK stimulation.
    1 context sentence
    Summary · context
    mdx mice were treated with the AMP-activated protein kinase (AMPK) activator 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside (AICAR; 500 mg·kg(-1)·day(-1)) for 30 days, and then one-half of the animals were subjected to a bout of treadmill running to induce acute AMPK and p38 MAPK signaling.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In mdx mice, chronic AICAR blunted stress-evoked SIRT1 expression compared with vehicle-treated mice.

    In plain wordsIn mice with muscular dystrophy, chronic AICAR blunted stress-evoked SIRT1 expression versus vehicle.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseSIRT1 expression
    Study

    mousen: not reported in source

    mdx dystrophic skeletal muscle
    Comparator
    Vehicle-treated mice
    Outcome group
    Receptor activity and mechanism · Musculoskeletal
    Studied dose
    500 mg·kg(-1)·day(-1) · 30 daysAs given in this study (mouse).

    Source sentences

    Summary
    Similarly, acute stress-evoked expression of PPARδ, PGC-1α, and SIRT1 was also blunted by chronic pharmacological AMPK stimulation.
    1 context sentence
    Summary · context
    mdx mice were treated with the AMP-activated protein kinase (AMPK) activator 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside (AICAR; 500 mg·kg(-1)·day(-1)) for 30 days, and then one-half of the animals were subjected to a bout of treadmill running to induce acute AMPK and p38 MAPK signaling.
  6. 06AnimalAnimal study (in vivo)Mechanism

    In mdx mice, AICAR attenuated running-evoked PRMT1 mRNA induction compared with vehicle-treated mice.

    In plain wordsIn mice with muscular dystrophy, AICAR reduced running-evoked PRMT1 mRNA induction versus vehicle.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreasePRMT1 mRNA induction
    Study

    mousen: not reported in source

    mdx dystrophic skeletal muscle
    Comparator
    Vehicle-treated mice
    Outcome group
    Receptor activity and mechanism · Musculoskeletal
    Studied dose
    500 mg·kg(-1)·day(-1) · 30 daysAs given in this study (mouse).

    Source sentences

    Summary
    The acute running-evoked induction of PRMT1 and CARM1 mRNAs was also attenuated by the AICAR treatment.
    1 context sentence
    Summary · context
    mdx mice were treated with the AMP-activated protein kinase (AMPK) activator 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside (AICAR; 500 mg·kg(-1)·day(-1)) for 30 days, and then one-half of the animals were subjected to a bout of treadmill running to induce acute AMPK and p38 MAPK signaling.
  7. 07AnimalAnimal study (in vivo)Mechanism

    In mdx mice, AICAR attenuated running-evoked CARM1 mRNA induction compared with vehicle-treated mice.

    In plain wordsIn mice with muscular dystrophy, AICAR reduced running-evoked CARM1 mRNA induction versus vehicle.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseCARM1 mRNA induction
    Study

    mousen: not reported in source

    mdx dystrophic skeletal muscle
    Comparator
    Vehicle-treated mice
    Outcome group
    Receptor activity and mechanism · Musculoskeletal
    Studied dose
    500 mg·kg(-1)·day(-1) · 30 daysAs given in this study (mouse).

    Source sentences

    Summary
    The acute running-evoked induction of PRMT1 and CARM1 mRNAs was also attenuated by the AICAR treatment.
    1 context sentence
    Summary · context
    mdx mice were treated with the AMP-activated protein kinase (AMPK) activator 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside (AICAR; 500 mg·kg(-1)·day(-1)) for 30 days, and then one-half of the animals were subjected to a bout of treadmill running to induce acute AMPK and p38 MAPK signaling.

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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