Population
Human aortic smooth muscle cells and wild-type/eNOS knockout mice
Comparison
NO donor DETA-NO and treadmill exercise training vs Untreated cells and non-exercised mice
Design
Preclinical
Authors
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Highlights potential vascular benefits of exercise via eNOS-ecSOD pathway; leaves open whether findings extend to human cardiovascular disease.
Endothelium-derived nitric oxide upregulates ecSOD expression, mediating the exercise-induced increase in ecSOD and potentially preventing NO degradation.
Fukai et al. (2000) studied this question.
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