Telmisartan suppresses cardiac hypertrophy by inhibiting cardiomyocyte apoptosis via the NFAT/ANP/BNP signaling pathway

Li,Xiurong; Lan,Yuhuai; Wang,Yan; Nie,Minghao; Lu,Yanhong; Zhao,Eryang

doi:10.3892/mmr.2017.6318

Telmisartan suppresses cardiac hypertrophy by inhibiting cardiomyocyte apoptosis via the NFAT/ANP/BNP signaling pathway

Authors:
- Xiurong Li
- Yuhuai Lan
- Yan Wang
- Minghao Nie
- Yanhong Lu
- Eryang Zhao
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Affiliations: Department of Pathology, Heilongjiang Provincial Hospital, Harbin, Heilongjiang 150036, P.R. China, Intensive Care Unit, Heilongjiang Provincial Hospital, Harbin, Heilongjiang 150036, P.R. China, Department of Oral Pathology, Stomatological Hospital, Harbin Medical University, Harbin, Heilongjiang 150036, P.R. China
Published online on: March 14, 2017 https://doi.org/10.3892/mmr.2017.6318
Pages: 2574-2582
Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Telmisartan, a type of angiotensin II (Ang II) receptor inhibitor, is a common agent used to treat hypertension in the clinic. Hypertension increases cardiac afterload and promotes cardiac hypertrophy. However, the ventricular Ang II receptor may be activated in the absence of hypertension. Therefore, telmisartan may reduce cardiac hypertrophy by indirectly ameliorating hypertensive symptoms and directly inhibiting the cardiac Ang II receptor. Nuclear factor of activated T‑cells (NFAT) contributes to cardiac hypertrophy via nuclear translocation, which induces a cascade of atrial natriuretic peptide (ANP) and brain/B‑type natriuretic peptide (BNP) expression and cardiomyocyte apoptosis. However, NFAT-mediated inhibition of cardiac hypertrophy by telmisartan remains poorly understood. The present study demonstrated that telmisartan suppressed cardiomyocyte hypertrophy in a mouse model of cardiac afterload and in cultured cardiomyocytes by inhibiting NFAT nuclear translocation, as well as by inhibiting ANP and BNP expression and cardiomyocyte apoptosis, in a dose‑dependent manner. The present study provides a novel insight into the potential underlying mechanisms of telmisartan-induced inhibition of cardiomyocyte hypertrophy, which involves inhibition of NFAT activation, nuclear translocation and the ANP/BNP cascade.

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