Exercise Training Has Contrasting Effects in Myocardial Infarction and Pressure Overload Due to Divergent Endothelial Nitric Oxide Synthase Regulation
| العنوان: | Exercise Training Has Contrasting Effects in Myocardial Infarction and Pressure Overload Due to Divergent Endothelial Nitric Oxide Synthase Regulation |
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| المؤلفون: | Dirk J. Duncker, Elza D. van Deel, Yanti Octavia, Monique C. de Waard, Martine de Boer |
| المساهمون: | RS: CARIM - R2.01 - Clinical atrial fibrillation, Promovendi CD, Cardiologie, Cardiology |
| المصدر: | International Journal of Molecular Sciences, Vol 19, Iss 7, p 1968 (2018) International Journal of Molecular Sciences International journal of molecular sciences, 19(7):1968. Multidisciplinary Digital Publishing Institute (MDPI) Volume 19 Issue 7 International Journal of Molecular Sciences, 19(7):1968. Multidisciplinary Digital Publishing Institute (MDPI) |
| بيانات النشر: | Multidisciplinary Digital Publishing Institute (MDPI), 2018. |
| سنة النشر: | 2018 |
| مصطلحات موضوعية: | 0301 basic medicine, CONGENITAL AORTIC-STENOSIS, Left, Aortic Valve Stenosis/enzymology, 030204 cardiovascular system & hematology, medicine.disease_cause, Inbred C57BL, Ventricular Function, Left, DISEASE, RECOMMENDATIONS, Superoxide Dismutase/metabolism, lcsh:Chemistry, chemistry.chemical_compound, Mice, 0302 clinical medicine, Superoxide Dismutase-1, Enos, Fibrosis, AMERICAN-HEART-ASSOCIATION, oxidative stress, FAILURE, Ventricular Function, Myocardial infarction, CARDIAC-HYPERTROPHY, lcsh:QH301-705.5, Spectroscopy, biology, exercise, Superoxide, nitric oxide synthase, ENOS, General Medicine, Physical Conditioning, Computer Science Applications, Superoxide Dismutase-1/metabolism, Nitric oxide synthase, myocardial infarction, Echocardiography, Cardiology, cardiovascular system, SKELETAL-MUSCLE, HEALTH, medicine.medical_specialty, Nitric Oxide Synthase Type III, Motor Activity, Nitric Oxide, Catalysis, Article, Nitric oxide, Myocardial Infarction/enzymology, Inorganic Chemistry, 03 medical and health sciences, Internal medicine, Physical Conditioning, Animal, medicine, Animals, Physical and Theoretical Chemistry, Molecular Biology, Pressure overload, business.industry, Superoxide Dismutase, Animal, Organic Chemistry, aortic stenosis, Nitric Oxide Synthase Type III/metabolism, Aortic Valve Stenosis, medicine.disease, biology.organism_classification, Mice, Inbred C57BL, Disease Models, Animal, 030104 developmental biology, PHYSICAL-ACTIVITY, chemistry, lcsh:Biology (General), lcsh:QD1-999, Nitric Oxide/metabolism, Disease Models, biology.protein, Sedentary Behavior, business, Oxidative stress |
| الوصف: | 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. |
| وصف الملف: | application/pdf |
| اللغة: | English |
| تدمد: | 1422-0067 1661-6596 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::995bd0fff58c81a51d74aa50a010e5b2Test https://doi.org/10.3390/ijms19071968Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....995bd0fff58c81a51d74aa50a010e5b2 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 14220067 16616596 |
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