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Minerva Cardioangiologica 2015 December;63(6):507-14

Copyright © 2015 EDIZIONI MINERVA MEDICA

lingua: Inglese

Telmisartan inhibited angiotensin II-induced collagen metabolic imbalance without directly targeting TGF-β 1/Smad signaling pathway in cardiac fibroblasts

Zhang Y. 1, Zhao N. A. 1, Wang J. K. 1, Zhu S. M. 1, Zhu H. L. 1, Liu B. 1, Cui Q. W. 1, Guan G. C. 1, Tian G. 2

1 First Department of Cardiology, Shaanxi Provincial People’s Hospital, Third Affiliated Hospital of Medical College of Xi'an Jiaotong University, Xi’an, Shaanxi, China; 2 Department of Cardiovascular Medicine, First Affiliated Hospital of Medical College of Xi'an Jiaotong University, Xi’an, Shaanxi, China


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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-β 1/Smad signaling molecule is an important pathway to achieve this effect. The aim of the study was to clarify whether, with excessive activation of RAAS system, telmisartan could also directly target TGF-β 1/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-β 1 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-β 1-induced cardiac fibroblasts. It was further confirmed by western blot method that telmisartan could inhibit TGF-β 1/Smad signaling molecule expression under the effect of Ang II, but telmisartan had no effect on TGF-β 1-induced Smad signaling molecule expression.
CONCLUSION: According to the present study telmisartan played a role of anticardiac fibrosis without directly targeting TGF-β 1/Smad signaling pathway molecule.

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