ArticleOxidative medicine and cellular longevity2017
High-Intensity Exercise Reduces Cardiac Fibrosis and Hypertrophy but Does Not Restore the Nitroso-Redox Imbalance in Diabetic Cardiomyopathy.
Article in Oxidative medicine and cellular longevity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 76 citations in OpenAlex.
- Impact of continuous vs. interval training on oxygen extraction and cardiac function during exercise in type 2 diabetes mellitus.European journal of applied physiology · 2022Trial
- Oxidative Stress in Diabetic Cardiomyopathy: Molecular Mechanisms, Current Treatment and Therapeutic Potential of Plant Antioxidants.Antioxidants (Basel, Switzerland) · 2026Review
- High intensity interval training and dalteparin attenuate doxorubicin induced cardiac damage and FoxO4 protein level in rats.Scientific reports · 2025Article
- High-intensity interval training (HIIT) ameliorates cardiac hypertrophy and fibrosis in diabetic rats: the role of P53 and SIRT1.Journal of molecular histology · 2025Article
- Beyond conventional therapy: NOX4 as a promising target in cardiomyopathy.Molecular biology reports · 2025Review
- Exercise and dietary interventions in the management of diabetic cardiomyopathy: mechanisms and implications.Cardiovascular diabetology · 2025Review
- Exercise in Diabetic Cardiomyopathy: Its Protective Effects and Molecular Mechanism.International journal of molecular sciences · 2025Review
- Physical Exercise: A Promising Treatment Against Organ Fibrosis.International journal of molecular sciences · 2025Review
- Mitochondria and NLRP3 inflammasome in cardiac hypertrophy.Molecular and cellular biochemistry · 2024Review
- Endurance Exercise Prevented Diabetic Cardiomyopathy through the Inhibition of Fibrosis and Hypertrophy in Rats.Reviews in cardiovascular medicine · 2024Article
- ATP releasing channels and the ameliorative effects of high intensity interval training on diabetic heart: a multifaceted analysis.Scientific reports · 2024Article
- Highlighting the effects of high-intensity interval training on the changes associated with hypertrophy, apoptosis, and histological proteins of the heart of old rats with type 2 diabetes.Scientific reports · 2024Article
- Diabetic Cardiomyopathy Uncovered: Transcriptomics, NLRP3, and Carvedilol Mechanisms.Journal of diabetes research · 2024Article
- Swimming alleviates myocardial fibrosis of type II diabetic rats through activating miR-34a-mediated SIRT1/PGC-1α/FNDC5 signal pathway.PloS one · 2024Article
- Nox4 as a novel therapeutic target for diabetic vascular complications.Redox biology · 2023Review
- Hypermethylation of ACADVL is involved in the high-intensity interval training-associated reduction of cardiac fibrosis in heart failure patients.Journal of translational medicine · 2023Article
- Highlighting the novel effects of high-intensity interval training on some histopathological and molecular indices in the heart of type 2 diabetic rats.Frontiers in endocrinology · 2023Article
- Decreased Cardiac NOX4 and SIRT-1 Protein Levels Contribute to Decreased Angiogenesis in the Heart of Diabetic Rats: Rescue Effects of IGF-1 and Exercise.Advanced pharmaceutical bulletin · 2023Article
- Rediscovering the value of exercise in patients with hypertrophic cardiomyopathy.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2022Review
- Tetrahydrobiopterin (BHBiomedicines · 2022Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic cardiomyopathy refers to the manifestations in the heart as a result of altered glucose homeostasis, reflected as fibrosis, cellular hypertrophy, increased oxidative stress, and apoptosis, leading to ventricular dysfunction. Since physical exercise has been indicated as cardioprotective, we tested the hypothesis that high-intensity exercise training could reverse the cardiac maladaptations produced by diabetes. For this, diabetes was induced in rats by a single dose of alloxan. Diabetic rats were randomly assigned to a sedentary group or submitted to a program of exercise on a treadmill for 4 weeks at 80% of maximal performance. Another group of normoglycemic rats was used as control. Diabetic rat hearts presented cardiomyocyte hypertrophy and interstitial fibrosis. Chronic exercise reduced both parameters but increased apoptosis. Diabetes increased the myocardial levels of the mRNA and proteins of NADPH oxidases NOX2 and NOX4. These altered levels were not reduced by exercise. Diabetes also increased the level of uncoupled endothelial nitric oxide synthase (eNOS) that was not reversed by exercise. Finally, diabetic rats showed a lower degree of phosphorylated phospholamban and reduced levels of SERCA2 that were not restored by high-intensity exercise. These results suggest that high-intensity chronic exercise was able to reverse remodeling in the diabetic heart but was unable to restore the nitroso-redox imbalance imposed by diabetes.
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