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Study · In vitro (cells) · 2025

3 results

Mechanisms of aerobic exercise on doxorubicin-induced cardiomyocyte apoptosis: based on AMPK/PI3K/AKT signalling pathway

Zhao Q, Zhao X, Zhang X, Cong R, Chen X, Dong D, Sun M

Life sciences1 Sept 2025

PepBankPUB-95934681
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Summary

The text of this summary is not shown here, because the article license does not allow reuse.

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study3

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

  1. 01LabIn vitro (cells)Mechanism

    In Dox-injured H9c2 cardiomyocytes, AICAR reduced apoptosis.

    In plain wordsIn cells injured by Dox, AICAR reduced cell death.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseCardiomyocyte apoptosis
    Study

    n: not reported in source

    Dox-injured H9c2 cardiomyocytes
    Outcome group
    Cell viability and death · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vitro, the AICAR reduced Dox-induced cardiomyocyte apoptosis and promoted cardiomyocyte proliferation by activating the PI3K/AKT signalling pathway.
    2 context sentences
    Summary · context
    In addition, an in vitro model of Dox-induced cardiomyocyte injury was established by using H9c2 cells.
    Summary · context
    Cells were treated with 5-Aminoimidazole-4-carboxamide ribonucleoside (AICAR, AMPK activator) and 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (LY294002, PI3K inhibitor), and cardiomyocyte apoptosis, proliferation, as well as the activity of PI3K/AKT pathway were evaluated.
  2. 02LabIn vitro (cells)Mechanism

    In Dox-injured H9c2 cardiomyocytes, AICAR promoted proliferation.

    In plain wordsIn cells injured by Dox, AICAR increased cell proliferation.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseCardiomyocyte proliferation
    Study

    n: not reported in source

    Dox-injured H9c2 cardiomyocytes
    Outcome group
    Cell proliferation and differentiation · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vitro, the AICAR reduced Dox-induced cardiomyocyte apoptosis and promoted cardiomyocyte proliferation by activating the PI3K/AKT signalling pathway.
    2 context sentences
    Summary · context
    In addition, an in vitro model of Dox-induced cardiomyocyte injury was established by using H9c2 cells.
    Summary · context
    Cells were treated with 5-Aminoimidazole-4-carboxamide ribonucleoside (AICAR, AMPK activator) and 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (LY294002, PI3K inhibitor), and cardiomyocyte apoptosis, proliferation, as well as the activity of PI3K/AKT pathway were evaluated.
  3. 03LabIn vitro (cells)Mechanism

    In Dox-injured H9c2 cardiomyocytes, AICAR activated the PI3K/AKT signaling pathway.

    In plain wordsIn cells injured by Dox, AICAR activated the PI3K/AKT pathway.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreasePI3K/AKT pathway activation
    Study

    n: not reported in source

    Dox-injured H9c2 cardiomyocytes
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vitro, the AICAR reduced Dox-induced cardiomyocyte apoptosis and promoted cardiomyocyte proliferation by activating the PI3K/AKT signalling pathway.
    2 context sentences
    Summary · context
    In addition, an in vitro model of Dox-induced cardiomyocyte injury was established by using H9c2 cells.
    Summary · context
    Cells were treated with 5-Aminoimidazole-4-carboxamide ribonucleoside (AICAR, AMPK activator) and 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (LY294002, PI3K inhibitor), and cardiomyocyte apoptosis, proliferation, as well as the activity of PI3K/AKT pathway were evaluated.

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

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