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Crim1 suppresses left ventricular hypertrophy. | LitMetric

Crim1 suppresses left ventricular hypertrophy.

Biomed Rep

Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA.

Published: June 2019

AI Article Synopsis

  • - Left ventricular hypertrophy (LVH) is a major contributor to heart failure and can lead to sudden death; Crim1, a protein that regulates heart development, might help prevent LVH. - In experiments with rat heart cells and models, it was found that Crim1 expression decreases during hypertrophy, while blocking a specific receptor with telmisartan increases Crim1 levels and inhibits hypertrophy. - The study suggests that enhancing Crim1 expression through treatment can effectively suppress ventricular hypertrophy, indicating its potential as a new target for heart disease therapies.

Article 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 and 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 . The overexpression of Crim1 by gavage with AT1R inhibitor telmisartan or myocardial injection of Ad-Crim1 markedly suppressed AAC-induced left ventricular hypertrophy . 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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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6566627PMC
http://dx.doi.org/10.3892/br.2019.1214DOI Listing

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