We have located links that may give you full text access.
The role of sildenafil in the development of transplant arteriosclerosis in rat aortic grafts.
Chronic rejection (CR), which is characterized histologically by progressive graft arteriosclerosis, remains a significant barrier to the long-term survival of a graft. Sildenafil has been shown to protect vascular endothelial cells. In this study, we found that sildenafil significantly reduces the thickness of transplant vascular intima in a rat aortic transplant model. Moreover, sildenafil dramatically decreased the expression of transforming growth factor-β1 (TGF-β1), vascular endothelial growth factor (VEGF), and α-smooth muscle actin (α-SMA) in the grafted aortas and increased the concentrations of cyclic guanosine monophosphate (cGMP) and endothelial nitric oxide synthase (eNOS) in serum. Furthermore, the ratio of regulatory T (Treg) cells and the expression of FoxP3 were increased, and the ratio of Th17 cells was decreased in the sildenafil-treated group. These results demonstrate that sildenafil enhances nitric oxide (NO) signaling by increasing the availability of cGMP, leading to an increase in the ratio of Treg/Th17 cells to attenuate transplant arteriosclerosis in a rat aortic transplant model.
Full text links
Related Resources
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app