Key result
Low-intensity pulsed ultrasound therapy ameliorated eNOS expression and its downstream pathway in 2 animal models of right ventricular failure.
Why the study?
Right ventricular failure is a leading cause of death in pulmonary hypertension, but effective treatment remains to be developed.
Does low-intensity pulsed ultrasound therapy improve eNOS expression and its downstream pathway in animal models of right ventricular failure?
Does low-intensity pulsed ultrasound therapy improve eNOS expression and its downstream pathway in animal models of right ventricular failure?
Low-intensity pulsed ultrasound therapy ameliorates eNOS expression and its downstream pathway in animal models of right ventricular failure, suggesting a potential novel therapeutic approach.
Answers are grounded in this paper and cite their sources.
May support ultrasound for RVF in preclinical models; leaves open translation to patients.
Right ventricular failure (RVF) is a leading cause of death in patients with pulmonary hypertension; however, effective treatment remains to be developed. We have developed low-intensity pulsed ultrasound therapy for cardiovascular diseases. In this study, we demonstrated that the expression of endothelial nitric oxide synthase (eNOS) in RVF patients was downregulated and that eNOS expression and its downstream pathway were ameliorated through eNOS activation in 2 animal models of RVF. These results indicate that eNOS is an important therapeutic target of RVF, for which low-intensity pulsed ultrasound therapy is a promising therapy for patients with RVF.
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Nakata et al. (2022) studied Right ventricular failure. Low-intensity pulsed ultrasound therapy was evaluated on eNOS expression and its downstream pathway. Low-intensity pulsed ultrasound therapy ameliorated eNOS expression and its downstream pathway in 2 animal models of right ventricular failure.
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