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Study · In vitro (cells) · 2022

3 results

Irisin and ALCAT1 mediated aerobic exercise-alleviated oxidative stress and apoptosis in skeletal muscle of mice with myocardial infarction.

Ren W, Xu Z, Pan S, Ma Y, Li H, Wu F, Bo W, Cai M, Tian Z

Free radical biology & medicine3 Nov 2022Cited by 30 (Europe PMC)

PMID36336228 (opens in a new tab)DOI10.1016/j.freeradbiomed.2022.10.321 (opens in a new tab)PepBankPUB-36336228
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 study3

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

  1. 01LabIn vitro (cells)Mechanism

    In C2C12 cells, AICAR intervention inhibited ALCAT1 expression induced by H2O2 or LV-Alcat1.

    In plain wordsIn cells, AICAR inhibited ALCAT1 expression induced by hydrogen peroxide or LV-Alcat1.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseALCAT1 expression
    Study

    n: not reported in source

    C2C12 cells exposed to H2O2 or LV-Alcat1
    Outcome group
    Receptor activity and mechanism · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    rhIrisin and AICAR intervention inhibited ALCAT1 expression, oxidative stress and cell apoptosis, which induced by H2O2 or LV-Alcat1 in C2C12 cells.
    1 context sentence
    Summary · context
    C2C12 cells were treated with H2O2 and recombinant human Irisin (rhIrisin), or transduced with a lentiviral vector to mediate the overexpression of ALCAT1 (LV-Alcat1).
  2. 02LabIn vitro (cells)Mechanism

    In C2C12 cells, AICAR intervention inhibited oxidative stress induced by H2O2 or LV-Alcat1.

    In plain wordsIn cells, AICAR inhibited oxidative stress induced by hydrogen peroxide or LV-Alcat1.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseOxidative stress
    Study

    n: not reported in source

    C2C12 cells exposed to H2O2 or LV-Alcat1
    Outcome group
    Oxidative stress · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    rhIrisin and AICAR intervention inhibited ALCAT1 expression, oxidative stress and cell apoptosis, which induced by H2O2 or LV-Alcat1 in C2C12 cells.
    1 context sentence
    Summary · context
    C2C12 cells were treated with H2O2 and recombinant human Irisin (rhIrisin), or transduced with a lentiviral vector to mediate the overexpression of ALCAT1 (LV-Alcat1).
  3. 03LabIn vitro (cells)Mechanism

    In C2C12 cells, AICAR intervention inhibited apoptosis induced by H2O2 or LV-Alcat1.

    In plain wordsIn cells, AICAR inhibited cell death induced by hydrogen peroxide or LV-Alcat1.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseCell apoptosis
    Study

    n: not reported in source

    C2C12 cells exposed to H2O2 or LV-Alcat1
    Outcome group
    Muscle injury and repair · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    rhIrisin and AICAR intervention inhibited ALCAT1 expression, oxidative stress and cell apoptosis, which induced by H2O2 or LV-Alcat1 in C2C12 cells.
    1 context sentence
    Summary · context
    C2C12 cells were treated with H2O2 and recombinant human Irisin (rhIrisin), or transduced with a lentiviral vector to mediate the overexpression of ALCAT1 (LV-Alcat1).

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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