ArticleOxidative medicine and cellular longevity2016
Exercise Training Attenuates Upregulation of p47(phox) and p67(phox) in Hearts of Diabetic Rats.
Article in Oxidative medicine and cellular longevity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Exercise Empowerment: A Multifaceted Anatomy in Managing Diabetic Myocardial Disorder.Journal of cardiovascular translational research · 2025Review
- Exercise and dietary interventions in the management of diabetic cardiomyopathy: mechanisms and implications.Cardiovascular diabetology · 2025Review
- Sodium-Glucose Cotransporter 2 Inhibitors as Potential Antioxidant Therapeutic Agents in Cardiovascular and Renal Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- Endurance Exercise Prevented Diabetic Cardiomyopathy through the Inhibition of Fibrosis and Hypertrophy in Rats.Reviews in cardiovascular medicine · 2024Article
- Effect of exercise on improving myocardial mitochondrial function in decreasing diabetic cardiomyopathy.Experimental physiology · 2024Review
- Effects of a Red Orange and Lemon Extract in Obese Diabetic Zucker Rats: Role of Nicotinamide Adenine Dinucleotide Phosphate Oxidase.Journal of clinical medicine · 2020Article
- Resistance Exercise Modulates Oxidative Stress Parameters and TNF-α Content in the Heart of Mice with Diet-Induced Obesity.Arquivos brasileiros de cardiologia · 2019Article
- High-Intensity Exercise Reduces Cardiac Fibrosis and Hypertrophy but Does Not Restore the Nitroso-Redox Imbalance in Diabetic Cardiomyopathy.Oxidative medicine and cellular longevity · 2017Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Exercise training (ExT) is currently being used as a nonpharmacological strategy to improve cardiac function in diabetic patients. However, the molecular mechanism(s) underlying its beneficial effects remains poorly understood. Oxidative stress is known to play a key role in the pathogenesis of diabetic cardiomyopathy and one of the enzyme systems that produce reactive oxygen species is NADH/NADPH oxidase. The goal of this study was to investigate the effect of streptozotocin- (STZ-) induced diabetes on expression of p47(phox) and p67(phox), key regulatory subunits of NADPH oxidase, in cardiac tissues and determine whether ExT can attenuate these changes. Four weeks after STZ treatment, expression of p47(phox) and p67(phox) increased 2.3-fold and 1.6-fold, respectively, in left ventricles of diabetic rats and these increases were attenuated with three weeks of ExT, initiated 1 week after onset of diabetes. In atrial tissues, there was increased expression of p47(phox) (74%), which was decreased by ExT in diabetic rats. Furthermore, increased collagen III levels in diabetic hearts (52%) were significantly reduced by ExT. Taken together, ExT attenuates the increased expression of p47(phox) and p67(phox) in the hearts of diabetic rats which could be an underlying mechanism for improving intracardiac matrix and thus cardiac function and prevent cardiac remodeling in diabetic cardiomyopathy.
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