ArticleInternational journal of molecular sciences2018
Exercise Training Has Contrasting Effects in Myocardial Infarction and Pressure Overload Due to Divergent Endothelial Nitric Oxide Synthase Regulation.
Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 17 citations in OpenAlex.
- Metabolic Remodeling Induced by Exercise: Emerging Mechanisms for Myocardial Protection in Cardiovascular Disease.Journal of cardiovascular translational research · 2026Review
- Left Ventricular Remodeling After Myocardial Infarction-Pathophysiology, Diagnostic Approach and Management During Cardiac Rehabilitation.International journal of molecular sciences · 2025Review
- Dietary intake of live microbes mitigates the mortality risk associated with sedentary behavior in US hypertensive individuals.Scientific reports · 2025Article
- Melanocortin 1 Receptor Regulates Pathological and Physiological Cardiac Remodeling.Journal of the American Heart Association · 2025Article
- Potential preservative mechanisms of cardiac rehabilitation pathways on endothelial function in coronary heart disease.Science China. Life sciences · 2025Review
- Article
- Aerobic Exercise Training Improves Calcium Handling and Cardiac Function in Rats with Heart Failure Resulting from Aortic Stenosis.International journal of molecular sciences · 2023Article
- Exercise training after myocardial infarction increases survival but does not prevent adverse left ventricle remodeling and dysfunction in high-fat diet fed mice.Life sciences · 2022Article
- Exercise Training after Myocardial Infarction Attenuates Dysfunctional Ventricular Remodeling and Promotes Cardiac Recovery.Reviews in cardiovascular medicine · 2022Review
- The Dysfunctional Scenario of the Major Components Responsible for Myocardial Calcium Balance in Heart Failure Induced by Aortic Stenosis.Arquivos brasileiros de cardiologia · 2022Article
- Structural and functional alterations in heart and skeletal muscle following severe TAC in mice: impact of moderate exercise training.Biological research · 2021Article
- Oxidative stress and inflammation contribute to traffic noise-induced vascular and cerebral dysfunction via uncoupling of nitric oxide synthases.Redox biology · 2020Review
- Exercise during transition from compensated left ventricular hypertrophy to heart failure in aortic stenosis rats.Journal of cellular and molecular medicine · 2019Article
- A systematic comparison of exercise training protocols on animal models of cardiovascular capacity.Life sciences · 2019Review
- New Therapeutic Implications of Endothelial Nitric Oxide Synthase (eNOS) Function/Dysfunction in Cardiovascular Disease.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The beneficial effects of exercise training (EX) on cardiac pathology are well recognized. Previously, we found that the effects of EX on cardiac dysfunction in mice critically depend on the underlying etiology. EX exerted beneficial effects after myocardial infarction (MI); however, cardiac pathology following pressure overload produced by transverse aortic constriction (TAC) was aggravated by EX. In the presented study, we investigated whether the contrasting effects of EX on cardiac dysfunction can be explained by an etiology-specific response of endothelial nitric oxide (NO) synthase (eNOS) to EX, which divergently affects the balance between nitric oxide and superoxide. For this purpose, mice were exposed to eight weeks of voluntary wheel running or sedentary housing (SED), immediately after sham, MI, or TAC surgery. Left ventricular (LV) function was assessed using echocardiography and hemodynamic measurements. EX ameliorated LV dysfunction and remodeling after MI, but not following TAC, in which EX even aggravated fibrosis. Strikingly, EX attenuated superoxide levels after MI, but exacerbated NOS-dependent superoxide levels following TAC. Similarly, elevated eNOS S-glutathionylation and eNOS monomerization, which were observed in both MI and TAC, were corrected by EX in MI, but aggravated by EX after TAC. Additionally, EX reduced antioxidant activity in TAC, while it was maintained following EX in MI. In conclusion, the present study shows that EX mitigates cardiac dysfunction after MI, likely by attenuating eNOS uncoupling-mediated oxidative stress, whereas EX tends to aggravate cardiac dysfunction following TAC, likely due to exacerbating eNOS-mediated oxidative stress.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.