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Study · In vitro (cells) · mouse · 2025

2 results

Molecular Mechanism of Aerobic Exercise Ameliorating Myocardial Mitochondrial Injury in Mice with Heart Failure.

Jia H, Song Y, Hua Y, Li K, Li S, Wang Y

International journal of molecular sciences27 Feb 2025Cited by 14 (Europe PMC)

PMID40076760 (opens in a new tab)PMCIDPMC11901053 (opens in a new tab)DOI10.3390/ijms26052136 (opens in a new tab)PepBankPUB-40076760
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Summary

To explore the molecular mechanism of aerobic exercise to improve heart failure and to provide a theoretical basis and experimental reference for the treatment of heart failure. Nine-week-old male mice were used to establish a left ventricular pressure overload-induced heart failure model by transverse aortic constriction (TAC). The mice were randomly divided into four groups: a sham group (SHAM), heart failure group (HF), heart failure + SKQ1 group (HS) and heart failure + aerobic exercise group (HE). The mice in the HE group were subjected to moderate-intensity aerobic exercise interventions. The mitochondrion-targeting antioxidant (SKQ1) contains the lipophilic cation TPP, which targets scavenging mitochondrial ROS. The HS group was subjected to SKQ1 (100 nmol/kg/d) interventions, which were initiated 1 week after the surgery, and the interventions lasted 8 weeks. Cardiac function was assessed by ultrasound, cardiomyocyte size by H&E and WGA staining, myocardial fibrosis by Masson's staining, and myocardial tissue oxidative stress and apoptosis by DHE and TUNEL fluorescence staining, respectively. Western blotting was used to detect the expression of mitochondrial quality control, inflammation, and apoptosis-related proteins. In the cellular level, an in vitro cellular model was established by isolating primary cardiomyocytes from neonatal mice (2-3 days) and intervening with Ang II (1 μM) to mimic heart failure. Oxidative stress and mitochondrial membrane potential were determined in the cardiomyocytes of each group by DHE and JC-1 staining, respectively. Myocardial fibrosis was increased significantly and cardiac function was reduced significantly in the heart failure mice. Aerobic exercise and SKQ1 intervention improved cardiac function and reduced myocardial hypertrophy and myocardial fibrosis in the heart failure mice significantly. Meanwhile, aerobic exercise and SKQ1 intervention reduced the number of DHE-positive particles (p p p p p p p < 0.01). In addition, the AMPK agonist AICAR and the mitochondria-targeted ROS scavenger (SKQ1) ameliorated AngII-induced mitochondrial fragmentation and decreased mitochondrial membrane potential in cardiomyocytes significantly. It was shown that inhibition of mitochondrial ROS by aerobic exercise, which in turn inhibits mitochondrial damage, improves mitochondrial quality control, and reduces myocardial inflammatory and apoptosis, may be an important molecular mechanism by which aerobic exercise exerts endogenous antioxidant protective effects to improve cardiac function.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study2

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

  1. 01LabIn vitro (cells)Efficacy outcome

    In neonatal mouse cardiomyocytes, AICAR significantly ameliorated AngII-induced mitochondrial fragmentation.

    In plain wordsIn cells from newborn mice, AICAR reduced mitochondrial fragmentation compared with AngII injury.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseMitochondrial fragmentation
    Study

    mousen: not reported in source

    Primary neonatal cardiomyocytes exposed to Ang II
    Comparator
    Ang II injury
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In addition, the AMPK agonist AICAR and the mitochondria-targeted ROS scavenger (SKQ1) ameliorated AngII-induced mitochondrial fragmentation and decreased mitochondrial membrane potential in cardiomyocytes significantly.
    1 context sentence
    Summary · context
    In the cellular level, an in vitro cellular model was established by isolating primary cardiomyocytes from neonatal mice (2-3 days) and intervening with Ang II (1 μM) to mimic heart failure.
  2. 02LabIn vitro (cells)Efficacy outcome

    In neonatal mouse cardiomyocytes, AICAR significantly ameliorated AngII-associated decreased mitochondrial membrane potential.

    In plain wordsIn cells from newborn mice, AICAR improved the reduced mitochondrial membrane potential associated with AngII injury.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseMitochondrial membrane potential
    Study

    mousen: not reported in source

    Primary neonatal cardiomyocytes exposed to Ang II
    Comparator
    Ang II injury
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In addition, the AMPK agonist AICAR and the mitochondria-targeted ROS scavenger (SKQ1) ameliorated AngII-induced mitochondrial fragmentation and decreased mitochondrial membrane potential in cardiomyocytes significantly.
    1 context sentence
    Summary · context
    In the cellular level, an in vitro cellular model was established by isolating primary cardiomyocytes from neonatal mice (2-3 days) and intervening with Ang II (1 μM) to mimic heart failure.

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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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