Crim1 suppresses left ventricular hypertrophy Corrigendum in /10.3892/br.2019.1241

Yang,Long; He,Jionghong; Xia,Guiling; Yang,Jun; Tang,Qian; Yang,Yongyao; Deng,Jiusheng

doi:10.3892/br.2019.1214

Crim1 suppresses left ventricular hypertrophy

Corrigendum in: /10.3892/br.2019.1241

Authors:
- Long Yang
- Jionghong He
- Guiling Xia
- Jun Yang
- Qian Tang
- Yongyao Yang
- Jiusheng Deng
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Affiliations: Department of Cardiology, Guizhou Provincial People's Hospital, Guiyang, Guizhou 550002, P.R. China, Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA
Published online on: May 17, 2019 https://doi.org/10.3892/br.2019.1214
Pages: 343-350

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Abstract

Left ventricular hypertrophy is a leading cause of heart failure and sudden death. Cysteine‑rich transmembrane bone morphogenetic protein regulator 1 (Crim1) is expressed at a high level in the heart and has a regulatory role in heart development. The present study aimed to test the hypothesis that Crim1 can have an inhibitory function on ventricular hypertrophy. Rat primary ventricular myocytes were stretched to induce myocyte hypertrophy, and treated with telmisartan or infected with Crim1‑expressing recombinant adenovirus (Ad‑Crim1). Rat ventricular hypertrophy was induced by abdominal aortic coarctation (AAC), and treated either with telmisartan or myocardial injection of Ad‑Crim1 or empty adenovirus vector. The results showed that the expression of Crim1 decreased in the hypertrophic ventricle. The inhibition of angiotensin receptor type 1 (AT1R) by telmisartan in vitro and in vivo significantly increased the expression of Crim1 in the left ventricle. The overexpression of Crim1 by infection with Ad‑Crim1 significantly inhibited stretch‑induced ventricular myocyte hypertrophy in vitro. The overexpression of Crim1 by gavage with AT1R inhibitor telmisartan or myocardial injection of Ad‑Crim1 markedly suppressed AAC‑induced left ventricular hypertrophy in vivo. These results suggest that Crim1 has a suppressive function on ventricular hypertrophy and provides a novel therapeutic target for the treatment of cardiac hypertrophy.

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