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Study · In vitro (cells) · 2013

8 results

AMPK attenuates microtubule proliferation in cardiac hypertrophy.

Fassett JT, Hu X, Xu X, Lu Z, Zhang P, Chen Y, Bache RJ

American journal of physiology. Heart and circulatory physiology11 Jan 2013Cited by 50 (Europe PMC)

PMID23316058 (opens in a new tab)PMCIDPMC3602754 (opens in a new tab)DOI10.1152/ajpheart.00935.2011 (opens in a new tab)PepBankPUB-23316058
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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 study8

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

  1. 01LabIn vitro (cells)Mechanism

    In neonatal cardiomyocytes, AICAR activation of AMPK attenuated phenylephrine-induced cell area enlargement.

    In plain wordsIn cells, AICAR reduced heart cell enlargement caused by phenylephrine.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseCardiomyocyte area
    Study

    n: not reported in source

    neonatal cardiomyocytes under hypertrophic stimulation
    Comparator
    hypertrophic stimulation without AMPK activation
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In neonatal cardiomyocytes, activation of AMPK with 5-aminoimidazole carboxamide ribonucleotide (AICAR) or expression of constitutively active AMPK (CA-AMPK) attenuated cell area increase by hypertrophic stimuli (phenylephrine).
  2. 02LabIn vitro (cells)Mechanism

    In neonatal cardiomyocytes, AICAR increased MAP4 Ser-915 phosphorylation, which reduces tubulin affinity and prevents microtubule stabilization.

    In plain wordsIn cells, AICAR increased MAP4 phosphorylation associated with reduced tubulin binding and microtubule stabilization.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseMAP4 Ser-915 phosphorylation
    Study

    n: not reported in source

    neonatal cardiomyocytes under hypertrophic stimulation
    Comparator
    hypertrophic stimulation without AMPK activation
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Mechanistically, AICAR treatment increased Ser-915 phosphorylation of microtubule-associated protein 4 (MAP4), which reduces affinity for tubulin and prevents stabilization of microtubules (MTs).
    1 context sentence
    Summary · context
    In neonatal cardiomyocytes, activation of AMPK with 5-aminoimidazole carboxamide ribonucleotide (AICAR) or expression of constitutively active AMPK (CA-AMPK) attenuated cell area increase by hypertrophic stimuli (phenylephrine).

Studies that did not test the peptide alone6

In this study, AICAR (acadesine) was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking AICAR (acadesine).

  1. 03LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Mechanism

    In neonatal cardiomyocytes, AMPK activation with AICAR or constitutively active AMPK expression had little effect on intermediate filaments.

    In plain wordsIn cells, AMPK activation with AICAR or gene expression had little effect on intermediate filaments.

    Peptide
    AICAR (acadesine)
    Outcome
    Direction not reportedIntermediate filaments
    Study

    n: not reported in source

    neonatal cardiomyocytes under hypertrophic stimulation
    Comparator
    hypertrophic stimulation without AMPK activation
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    AMPK activation had little effect on intermediate filaments or myofilaments but dramatically reduced microtubule stability, as measured by detyrosinated tubulin levels and cytoskeletal tubulin accumulation.
    1 context sentence
    Summary · context
    In neonatal cardiomyocytes, activation of AMPK with 5-aminoimidazole carboxamide ribonucleotide (AICAR) or expression of constitutively active AMPK (CA-AMPK) attenuated cell area increase by hypertrophic stimuli (phenylephrine).

    In this study, AICAR (acadesine) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking AICAR (acadesine).

  2. 04LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Mechanism

    In neonatal cardiomyocytes, AMPK activation with AICAR or constitutively active AMPK expression had little effect on myofilaments.

    In plain wordsIn cells, AMPK activation with AICAR or gene expression had little effect on muscle filaments.

    Peptide
    AICAR (acadesine)
    Outcome
    Direction not reportedMyofilaments
    Study

    n: not reported in source

    neonatal cardiomyocytes under hypertrophic stimulation
    Comparator
    hypertrophic stimulation without AMPK activation
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    AMPK activation had little effect on intermediate filaments or myofilaments but dramatically reduced microtubule stability, as measured by detyrosinated tubulin levels and cytoskeletal tubulin accumulation.
    1 context sentence
    Summary · context
    In neonatal cardiomyocytes, activation of AMPK with 5-aminoimidazole carboxamide ribonucleotide (AICAR) or expression of constitutively active AMPK (CA-AMPK) attenuated cell area increase by hypertrophic stimuli (phenylephrine).

    In this study, AICAR (acadesine) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking AICAR (acadesine).

  3. 05LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Mechanism

    In neonatal cardiomyocytes, AMPK activation with AICAR or constitutively active AMPK expression reduced microtubule stability measured by detyrosinated tubulin.

    In plain wordsIn cells, AMPK activation with AICAR or gene expression reduced microtubule stability measured by altered tubulin levels.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseDetyrosinated tubulin levels
    Study

    n: not reported in source

    neonatal cardiomyocytes under hypertrophic stimulation
    Comparator
    hypertrophic stimulation without AMPK activation
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    AMPK activation had little effect on intermediate filaments or myofilaments but dramatically reduced microtubule stability, as measured by detyrosinated tubulin levels and cytoskeletal tubulin accumulation.
    1 context sentence
    Summary · context
    In neonatal cardiomyocytes, activation of AMPK with 5-aminoimidazole carboxamide ribonucleotide (AICAR) or expression of constitutively active AMPK (CA-AMPK) attenuated cell area increase by hypertrophic stimuli (phenylephrine).

    In this study, AICAR (acadesine) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking AICAR (acadesine).

  4. 06LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Mechanism

    In neonatal cardiomyocytes, AMPK activation with AICAR or constitutively active AMPK expression reduced cytoskeletal tubulin accumulation.

    In plain wordsIn cells, AMPK activation with AICAR or gene expression reduced tubulin accumulation in the cell skeleton.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseCytoskeletal tubulin accumulation
    Study

    n: not reported in source

    neonatal cardiomyocytes under hypertrophic stimulation
    Comparator
    hypertrophic stimulation without AMPK activation
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    AMPK activation had little effect on intermediate filaments or myofilaments but dramatically reduced microtubule stability, as measured by detyrosinated tubulin levels and cytoskeletal tubulin accumulation.
    1 context sentence
    Summary · context
    In neonatal cardiomyocytes, activation of AMPK with 5-aminoimidazole carboxamide ribonucleotide (AICAR) or expression of constitutively active AMPK (CA-AMPK) attenuated cell area increase by hypertrophic stimuli (phenylephrine).

    In this study, AICAR (acadesine) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking AICAR (acadesine).

  5. 07LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Mechanism

    In neonatal cardiomyocytes, low-level AMPK activation limited cell expansion independently of mTORC1 or protein synthesis repression.

    In plain wordsIn cells, low-level AMPK activation limited heart cell expansion without depending on mTORC1 or protein synthesis inhibition.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseCell expansion under low-level AMPK activation
    Study

    n: not reported in source

    neonatal cardiomyocytes under hypertrophic stimulation
    Comparator
    hypertrophic stimulation without AMPK activation
    Outcome group
    Heart function · Cardiovascular

    Source sentences

    Summary
    Importantly, low-level AMPK activation limited cell expansion and microtubule growth independent of mTORC1 or protein synthesis repression, identifying a new mechanism by which AMPK regulates cell growth.
    1 context sentence
    Summary · context
    In neonatal cardiomyocytes, activation of AMPK with 5-aminoimidazole carboxamide ribonucleotide (AICAR) or expression of constitutively active AMPK (CA-AMPK) attenuated cell area increase by hypertrophic stimuli (phenylephrine).

    In this study, AICAR (acadesine) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking AICAR (acadesine).

  6. 08LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Mechanism

    In neonatal cardiomyocytes, low-level AMPK activation limited microtubule growth independently of mTORC1 or protein synthesis repression.

    In plain wordsIn cells, low-level AMPK activation limited microtubule growth without depending on mTORC1 or protein synthesis inhibition.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseMicrotubule growth under low-level AMPK activation
    Study

    n: not reported in source

    neonatal cardiomyocytes under hypertrophic stimulation
    Comparator
    hypertrophic stimulation without AMPK activation
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    Importantly, low-level AMPK activation limited cell expansion and microtubule growth independent of mTORC1 or protein synthesis repression, identifying a new mechanism by which AMPK regulates cell growth.
    1 context sentence
    Summary · context
    In neonatal cardiomyocytes, activation of AMPK with 5-aminoimidazole carboxamide ribonucleotide (AICAR) or expression of constitutively active AMPK (CA-AMPK) attenuated cell area increase by hypertrophic stimuli (phenylephrine).

    In this study, AICAR (acadesine) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking AICAR (acadesine).

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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