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Study · Animal study (in vivo) · rat · 2007

5 results

Long-term activation of adenosine monophosphate-activated protein kinase attenuates pressure-overload-induced cardiac hypertrophy.

Li HL, Yin R, Chen D, Liu D, Wang D, Yang Q, Dong YG

Journal of cellular biochemistry1 Apr 2007Cited by 105 (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 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 rats with transaortic constriction, long-term AICAR activation of AMPK attenuated cardiac hypertrophy.

    In plain wordsIn rats, AICAR reduced heart enlargement compared with pressure overload without AICAR.

    Outcome
    DecreaseCardiac hypertrophy
    Study

    ratn: not reported in source

    Transaortic constriction
    Comparator
    Pressure overload without AICAR
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    0.5 mg/g body wt · 7 weeksAs given in this study (rat).

    Source sentences

    Summary
    We found that long-term AMPK activation attenuated cardiac hypertrophy, and improved cardiac function in rats subjected to TAC.
    1 context sentence
    Summary · context
    To examine the effects of AMPK activation in the development of pressure overload-induced cardiac hypertrophy, we administered 5-aminoimidazole 1 carboxamide ribonucleoside (AICAR, 0.5 mg/g body wt), a specific activator of AMPK, to rats with transaortic constriction (TAC) for 7 weeks.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In rats with transaortic constriction, long-term AICAR activation of AMPK improved cardiac function.

    In plain wordsIn rats, AICAR improved heart function compared with pressure overload without AICAR.

    Outcome
    IncreaseCardiac function
    Study

    ratn: not reported in source

    Transaortic constriction
    Comparator
    Pressure overload without AICAR
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    0.5 mg/g body wt · 7 weeksAs given in this study (rat).

    Source sentences

    Summary
    We found that long-term AMPK activation attenuated cardiac hypertrophy, and improved cardiac function in rats subjected to TAC.
    1 context sentence
    Summary · context
    To examine the effects of AMPK activation in the development of pressure overload-induced cardiac hypertrophy, we administered 5-aminoimidazole 1 carboxamide ribonucleoside (AICAR, 0.5 mg/g body wt), a specific activator of AMPK, to rats with transaortic constriction (TAC) for 7 weeks.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In pressure-overloaded rat hearts, long-term AICAR activation of AMPK attenuated protein synthesis.

    In plain wordsIn rats, AICAR reduced heart protein production compared with pressure overload without AICAR.

    Outcome
    DecreaseCardiac protein synthesis
    Study

    ratn: not reported in source

    Transaortic constriction
    Comparator
    Pressure overload without AICAR
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    0.5 mg/g body wt · 7 weeksAs given in this study (rat).

    Source sentences

    Summary
    Furthermore, long-term AMPK activation attenuated protein synthesis, diminished calcineurin-nuclear factor of activated T cells (NFAT) and nuclear factor kappaB (NF-kappaB) signaling in pressure overload-induced hypertrophic hearts.
    1 context sentence
    Summary · context
    To examine the effects of AMPK activation in the development of pressure overload-induced cardiac hypertrophy, we administered 5-aminoimidazole 1 carboxamide ribonucleoside (AICAR, 0.5 mg/g body wt), a specific activator of AMPK, to rats with transaortic constriction (TAC) for 7 weeks.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In pressure-overloaded rat hearts, long-term AICAR activation of AMPK diminished calcineurin-NFAT signaling.

    In plain wordsIn rats, AICAR reduced calcineurin-NFAT signaling compared with pressure overload without AICAR.

    Outcome
    DecreaseCalcineurin-NFAT signaling
    Study

    ratn: not reported in source

    Transaortic constriction
    Comparator
    Pressure overload without AICAR
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    0.5 mg/g body wt · 7 weeksAs given in this study (rat).

    Source sentences

    Summary
    Furthermore, long-term AMPK activation attenuated protein synthesis, diminished calcineurin-nuclear factor of activated T cells (NFAT) and nuclear factor kappaB (NF-kappaB) signaling in pressure overload-induced hypertrophic hearts.
    1 context sentence
    Summary · context
    To examine the effects of AMPK activation in the development of pressure overload-induced cardiac hypertrophy, we administered 5-aminoimidazole 1 carboxamide ribonucleoside (AICAR, 0.5 mg/g body wt), a specific activator of AMPK, to rats with transaortic constriction (TAC) for 7 weeks.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In pressure-overloaded rat hearts, long-term AICAR activation of AMPK diminished NF-kappaB signaling.

    In plain wordsIn rats, AICAR reduced NF-kappaB signaling compared with pressure overload without AICAR.

    Outcome
    DecreaseNF-kappaB signaling
    Study

    ratn: not reported in source

    Transaortic constriction
    Comparator
    Pressure overload without AICAR
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    0.5 mg/g body wt · 7 weeksAs given in this study (rat).

    Source sentences

    Summary
    Furthermore, long-term AMPK activation attenuated protein synthesis, diminished calcineurin-nuclear factor of activated T cells (NFAT) and nuclear factor kappaB (NF-kappaB) signaling in pressure overload-induced hypertrophic hearts.
    1 context sentence
    Summary · context
    To examine the effects of AMPK activation in the development of pressure overload-induced cardiac hypertrophy, we administered 5-aminoimidazole 1 carboxamide ribonucleoside (AICAR, 0.5 mg/g body wt), a specific activator of AMPK, to rats with transaortic constriction (TAC) for 7 weeks.

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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