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Study · In vitro (cells) · 2024

3 results

Resistance exercise upregulates Irisin expression and suppresses myocardial fibrosis following myocardial infarction via activating AMPK-Sirt1 and inactivating TGFβ1-Smad2/3.

Li H, Qin S, Tang J, Wang T, Ren W, Di L, Bo W, Ma Y, Wu F, Xu Z, Song W, Cai M, Xi Y, Tian Z

Acta physiologica (Oxford, England)16 May 2024Cited by 25 (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 study3

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

  1. 01LabIn vitro (cells)Mechanism

    In hydrogen peroxide-treated cardiac fibroblasts, AICAR activated the AMPK-Sirt1 pathway.

    In plain wordsIn cells treated with hydrogen peroxide, AICAR activated the AMPK-Sirt1 pathway.

    Outcome
    IncreaseAMPK-Sirt1 pathway activation
    Study

    n: not reported in source

    Primary cardiac fibroblasts treated with hydrogen peroxide
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Results of the in vitro experiments showed that AICAR and rhIRISIN intervention activated the AMPK-Sirt1 pathway and inactivated the TGFβ1-Smad2/3 pathway, and promoted apoptosis in H2O2-treated CFs.
    1 context sentence
    Summary · context
    In addition, H2O2, AICAR, recombinant human Irisin protein (rhIRISIN), and Sirt1 shRNA lentivirus (LV-Sirt1 shRNA) were used to intervene primary isolated cardiac fibroblasts (CFs).
  2. 02LabIn vitro (cells)Mechanism

    In hydrogen peroxide-treated cardiac fibroblasts, AICAR inactivated the TGFβ1-Smad2/3 pathway.

    In plain wordsIn cells treated with hydrogen peroxide, AICAR inactivated the TGFβ1-Smad2/3 pathway.

    Outcome
    DecreaseTGFbeta1-Smad2/3 pathway activation
    Study

    n: not reported in source

    Primary cardiac fibroblasts treated with hydrogen peroxide
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Results of the in vitro experiments showed that AICAR and rhIRISIN intervention activated the AMPK-Sirt1 pathway and inactivated the TGFβ1-Smad2/3 pathway, and promoted apoptosis in H2O2-treated CFs.
    1 context sentence
    Summary · context
    In addition, H2O2, AICAR, recombinant human Irisin protein (rhIRISIN), and Sirt1 shRNA lentivirus (LV-Sirt1 shRNA) were used to intervene primary isolated cardiac fibroblasts (CFs).
  3. 03LabIn vitro (cells)Mechanism

    In hydrogen peroxide-treated cardiac fibroblasts, AICAR promoted apoptosis.

    In plain wordsIn cells treated with hydrogen peroxide, AICAR promoted cardiac fibroblast death.

    Outcome
    IncreaseCardiac fibroblast apoptosis
    Study

    n: not reported in source

    Primary cardiac fibroblasts treated with hydrogen peroxide
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Results of the in vitro experiments showed that AICAR and rhIRISIN intervention activated the AMPK-Sirt1 pathway and inactivated the TGFβ1-Smad2/3 pathway, and promoted apoptosis in H2O2-treated CFs.
    1 context sentence
    Summary · context
    In addition, H2O2, AICAR, recombinant human Irisin protein (rhIRISIN), and Sirt1 shRNA lentivirus (LV-Sirt1 shRNA) were used to intervene primary isolated cardiac fibroblasts (CFs).

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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