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Study · Not a test of the peptide alone · 2021

3 results

Exercise Training Alleviates Cardiac Fibrosis through Increasing Fibroblast Growth Factor 21 and Regulating TGF-β1-Smad2/3-MMP2/9 Signaling in Mice with Myocardial Infarction.

Ma Y, Kuang Y, Bo W, Liang Q, Zhu W, Cai M, Tian Z

International journal of molecular sciences15 Nov 2021Cited by 104 (Europe PMC)

PMID34830222 (opens in a new tab)PMCIDPMC8623999 (opens in a new tab)DOI10.3390/ijms222212341 (opens in a new tab)PepBankPUB-34830222
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Summary

Exercise training has been reported to alleviate cardiac fibrosis and ameliorate heart dysfunction after myocardial infarction (MI), but the molecular mechanism is still not fully clarified. Fibroblast growth factor 21 (FGF21) exerts a protective effect on the infarcted heart. This study investigates whether exercise training could increase FGF21 protein expression and regulate the transforming growth factor-β1 (TGF-β1)-Smad2/3-MMP2/9 signaling pathway to alleviate cardiac fibrosis following MI. Male wild type (WT) C57BL/6J mice and Fgf21 knockout (Fgf21 KO) mice were used to establish the MI model and subjected to five weeks of different types of exercise training. Both aerobic exercise training (AET) and resistance exercise training (RET) significantly alleviated cardiac dysfunction and fibrosis, up-regulated FGF21 protein expression, inhibited the activation of TGF-β1-Smad2/3-MMP2/9 signaling pathway and collagen production, and meanwhile, enhanced antioxidant capacity and reduced cell apoptosis in the infarcted heart. In contrast, knockout of Fgf21 weakened the cardioprotective effects of AET after MI. In vitro, cardiac fibroblasts (CFs) were isolated from neonatal mice hearts and treated with H2O2 (100 μM, 6 h). Recombinant human FGF21 (rhFGF21, 100 ng/mL, 15 h) and/or 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR, 1 mM, 15 h) inhibited H2O2-induced activation of the TGF-β1-Smad2/3-MMP2/9 signaling pathway, promoted CFs apoptosis and reduced collagen production. In conclusion, exercise training increases FGF21 protein expression, inactivates the TGF-β1-Smad2/3-MMP2/9 signaling pathway, alleviates cardiac fibrosis, oxidative stress, and cell apoptosis, and finally improves cardiac function in mice with MI. FGF21 plays an important role in the anti-fibrosis effect of exercise training.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study3

No result from this study comes from a test of the peptide.

Studies that did not test the peptide alone3

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. 01LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Mechanism

    In mouse cardiac fibroblasts, rhFGF21 and/or AICAR inhibited H2O2-induced TGF-β1-Smad2/3-MMP2/9 signaling.

    In plain wordsIn cells from mice, rhFGF21 and/or AICAR inhibited peroxide-induced signaling.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseTGF-β1-Smad2/3-MMP2/9 signaling
    Study

    mousen: not reported in source

    H2O2-treated neonatal cardiac fibroblasts
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    Recombinant human FGF21 (rhFGF21, 100 ng/mL, 15 h) and/or 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR, 1 mM, 15 h) inhibited H2O2-induced activation of the TGF-β1-Smad2/3-MMP2/9 signaling pathway, promoted CFs apoptosis and reduced collagen production.
    1 context sentence
    Summary · context
    In vitro, cardiac fibroblasts (CFs) were isolated from neonatal mice hearts and treated with H2O2 (100 μM, 6 h).

    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. 02LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Mechanism

    In mouse cardiac fibroblasts, rhFGF21 and/or AICAR promoted apoptosis.

    In plain wordsIn cells from mice, rhFGF21 and/or AICAR increased fibroblast death.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseFibroblast apoptosis
    Study

    mousen: not reported in source

    H2O2-treated neonatal cardiac fibroblasts
    Outcome group
    Cell viability and death · Cardiovascular

    Source sentences

    Summary
    Recombinant human FGF21 (rhFGF21, 100 ng/mL, 15 h) and/or 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR, 1 mM, 15 h) inhibited H2O2-induced activation of the TGF-β1-Smad2/3-MMP2/9 signaling pathway, promoted CFs apoptosis and reduced collagen production.
    1 context sentence
    Summary · context
    In vitro, cardiac fibroblasts (CFs) were isolated from neonatal mice hearts and treated with H2O2 (100 μM, 6 h).

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

    In mouse cardiac fibroblasts, rhFGF21 and/or AICAR reduced collagen production.

    In plain wordsIn cells from mice, rhFGF21 and/or AICAR reduced collagen production.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseCollagen production
    Study

    mousen: not reported in source

    H2O2-treated neonatal cardiac fibroblasts
    Outcome group
    Heart function · Cardiovascular

    Source sentences

    Summary
    Recombinant human FGF21 (rhFGF21, 100 ng/mL, 15 h) and/or 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR, 1 mM, 15 h) inhibited H2O2-induced activation of the TGF-β1-Smad2/3-MMP2/9 signaling pathway, promoted CFs apoptosis and reduced collagen production.
    1 context sentence
    Summary · context
    In vitro, cardiac fibroblasts (CFs) were isolated from neonatal mice hearts and treated with H2O2 (100 μM, 6 h).

    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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