Telmisartan inhibited angiotensin II-induced collagen metabolic imbalance without directly targeting TGF-β1/Smad signaling pathway in cardiac fibroblasts

Aim: Cardiac fibrosis is an important pathological process of cardiac remodeling. A large number of studies have shown that telmisartan can attenuate cardiac fibrosis through acting on angiotensin II 1 receptor (AT1R), and TGF-β1/Smad signaling molecule is an important pathway to achieve this effect. This study aims to clarify whether, with excessive activation of RAAS system, telmisartan could also directly target TGF-β1/Smad signaling pathway to have the function of anti-cardiac fibrosis. Methods: In this study, neonatal rat cardiac fibroblasts were cultured and AngII or TGF-β1 was administered for treatment or pre-incubation, and then telmisartan was used for 24 hours' incubation. Western blot and enzyme-linked immunosorbent assay (ELISA) tests were performed to detect protein expressions. Results: The results showed that telmisartan could inhibit collagen synthesis and collagen metabolic imbalance under the effect of Ang II, but telmisartan could not have such function in TGF-β1-induced cardiac fibroblasts. It was further confirmed by western blot method that telmisartan could inhibit TGF-β1/Smad signaling molecule expression under the effect of Ang II, but telmisartan had no effect on TGF-β1-induced Smad signaling molecule expression. Conclusion: This study found that telmisartan played role of anti-cardiac fibrosis without directly targeting TGF-β1/Smad signaling pathway molecule.