ArticleInternational journal of molecular sciences2025
Molecular Mechanism of Aerobic Exercise Ameliorating Myocardial Mitochondrial Injury in Mice with Heart Failure.
Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- Mitochondrial dysfunction and applications of mitochondrial-targeted delivery systems in atherosclerosis.Drug delivery · 2026Review
- Exercise-induced adipose tissue ADRB2-PGC1α-FGF21 signaling protects against pathological cardiac hypertrophy.iScience · 2026Article
- Molecular Mechanisms of Obesity-Associated Oxidative Stress and Therapeutic Strategies.Antioxidants (Basel, Switzerland) · 2026Review
- Exercise Training Across the Hypertensive Heart Disease Continuum: Clinical Evidence and Implications for Prescription.Journal of cardiovascular development and disease · 2026Review
- Early prediction of synergistic cardiotoxicity induced by PD-1 inhibitors and doxorubicin using cardiacChinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2026Article
- Mitochondrial Calcium Dysregulation and Targeted Therapies in Heart Failure.Reviews in cardiovascular medicine · 2026Review
- Mitochondrial dysfunction-driven PANoptosis in doxorubicin-induced cardiotoxicity: mechanistic insights and intervention strategies.Frontiers in pharmacology · 2026Review
- Oxidative Modifications in Cardiac Mitochondrial and CaHandbook of experimental pharmacology · 2026Review
- Physical exercise as a precision strategy for targeted PINK1 recruitment- a mechanistic review.Frontiers in physiology · 2026Review
- miR-17-5p Inhibits BNIP3-Mediated Mitochondrial Autophagy to Attenuate Pathological Cardiac FibrosisBalkan medical journal · 2025Article
- Molecular Insights into Oxidative-Stress-Mediated Cardiomyopathy and Potential Therapeutic Strategies.Biomolecules · 2025Review
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Authors and funding
6 authors.
Funding
Abstract
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 (
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