ArticleMolecular medicine reports2017
Telmisartan improves vascular remodeling through ameliorating prooxidant and profibrotic mechanisms in hypertension via the involvement of transforming growth factor-β1.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 22 citations in OpenAlex.
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- Network Pharmacology and In Vivo Analysis of Dahuang-Huangqi Decoction Effectiveness in Alleviating Renal Interstitial Fibrosis.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Study on the Potential Mechanism of Fructus Tribuli in the Treatment of Hypertensive Vascular Remodeling Based on Network Pharmacology and Molecular Docking.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- miR-126a-3p targets HIF-1α and alleviates obstructive sleep apnea syndrome with hypertension.Human cell · 2020Article
- The Role of Oxidative Stress in Physiopathology and Pharmacological Treatment with Pro- and Antioxidant Properties in Chronic Diseases.Oxidative medicine and cellular longevity · 2020Review
- Regulation of TGF-β1 on PI3KC3 and its role in hypertension-induced vascular injuries.Experimental and therapeutic medicine · 2019Article
- Inhibitory Effects of Roseoside and Icariside E4 Isolated from a Natural Product Mixture (No-ap) on the Expression of Angiotensin II Receptor 1 and Oxidative Stress in Angiotensin II-Stimulated H9C2 Cells.Molecules (Basel, Switzerland) · 2019Article
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12 authors at 3 institutions in 1 country.
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Abstract
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.
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