English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Vascular remodeling is a common complication and pathological basis of hypertension. Transforming growth factor‑β1 (TGF‑β1)/small mothers against decapentaplegic 3 (Smad3) is considered a potential therapeutic target for vascular remodeling in hypertension. The present study aimed to demonstrate the antifibrotic effects of telmisartan and examined the potential mechanisms associated with its prevention of vascular remodeling. Spontaneously hypertensive rats (SHRs) were treated with telmisartan (20 mg/kg), and vascular contractility, reactivity and oxidative stress were preliminarily evaluated. Vascular pathological alterations and collagen deposition were assessed using hematoxylin and eosin, and Masson staining, respectively. The profibrotic factors, TGF‑β1 and Smad3 were evaluated using immunofluorescence and immunohistochemistry. The protein levels of TGF‑β1/Smad3, phosphorylated (p‑)Smad3, collagen‑1 and α-smooth muscle actin in the aorta were assessed using western blot analysis. It was found that telmisartan attenuated chronic vasoconstriction and oxidative stress in the SHRs, and improved vascular reactivity. Telmisartan also restored vascular pathological alterations and decreased collagen deposition. In the vascular wall of the SHRs, telmisartan effectively decreased the protein levels of TGF‑β1/Smad3 and p‑Smad3. Taken together, these findings indicated that telmisartan, with its antioxidant effect, prevented vascular remodeling in hypertension through preventing the TGF‑β1/Smad3 signaling pathway.

molecular medicine reports

Telmisartan improves vascular remodeling through ameliorating prooxidant and profibrotic mechanisms in hypertension via the involvement of transforming growth factor-β1