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Helen E MacLean, Alison J Moore, Stephen A Sastra, Howard A Morris, Ali Ghasem-Zadeh, Kesha Rana, Anna-Maree Axell, Amanda J Notini, David J Handelsman, Ego Seeman, Jeffrey D Zajac, and Rachel A Davey

hypertrophy in vitro ( Marsh et al . 1998 ), and male mice that are AR null have small hearts, with a 14% decrease in heart weight/body weight ratio, and are susceptible to angiotensin II-induced cardiac remodeling ( Ikeda et al . 2005 ). In contrast, our

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I Stoykov, B Zandieh-Doulabi, A F M Moorman, V Christoffels, W M Wiersinga, and O Bakker

Introduction Tri-iodothyronine (T 3 ) affects cardiac function mainly by exerting a direct effect on cardiac cells through binding to thyroid hormone receptors (TR), thus regulating several functionally important proteins responsible

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Local impact of thyroid hormone inactivation

Deiodinases: the balance of thyroid hormone

Monica Dentice and Domenico Salvatore

have revealed the reexpression of D3 in different pathophysiological conditions, among which are cancer, cardiac hypertrophy, myocardial infarction (MI), chronic inflammation, and critical illness ( Gereben et al . 2008 b ). Because of its presence in

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Aiying Liu, Liping Gao, Shoulei Kang, Ying Liu, Chuanying Xu, Hong Sun, Dongye Li, and Changdong Yan

Collier ML Deng KY Jeyakumar LH Magnuson MA 2002 Oestrogen protects FKBP12.6 null mice from cardiac hypertrophy . Nature 6878 334 – 338 . doi:10.1038/416334a . Xu X De Pergola G Bjorntorp P 1991 Testosterone increases lipolysis

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Manon M Roustit, Joan M Vaughan, Pauline M Jamieson, and Mark E Cleasby

treatments available. However, recent work has demonstrated that generalised overexpression of urocortin 3 (UCN3) in mice results in both hypertrophy and increased glucose disposal into muscle ( Jamieson et al . 2011 ), making this an interesting candidate

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Milan Obradovic, Predrag Bjelogrlic, Manfredi Rizzo, Niki Katsiki, Mohamed Haidara, Alan J Stewart, Aleksandra Jovanovic, and Esma R Isenovic

concentration is decreased by up to 40% ( Norgaard et al . 1988 ). Semb et al . (1998) examined changes in cardiac Na + /K + -ATPase expression and function in a post-infarction rat model of hypertrophy and congestive HF (CHF). They found that in the CHF

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Gregory S Y Ong, Timothy J Cole, Gregory H Tesch, James Morgan, Jennifer K Dowling, Ashley Mansell, Peter J Fuller, and Morag J Young

al. 2014 a , Shen et al. 2014 ). Similarly, deletion of MR from cardiomyocytes or vascular endothelial cells revealed independent roles for MR in these cells for cardiac pathology, that is, macrophage recruitment and cellular hypertrophy ( Rickard

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Amanda E Garza, Elijah Trefts, Isis A Katayama Rangel, Danielle Brooks, Rene Baudrand, Burhanuddin Moize, Jose R Romero, Sanjay Ranjit, Thitinan Treesaranuwattana, Tham M Yao, Gail K Adler, Luminita H Pojoga, and Gordon H Williams

significantly reduced in the L-NAME/AngII treated WT mice compared to WT control mice. Striatin deficiency did not modify L-NAME/AngII induced cardiac injury As an assessment of cardiac hypertrophy, we measured the heart to body weight (BW) ratio. L

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Marina C Muñoz, Valeria Burghi, Johanna G Miquet, Jorge F Giani, Ricardo D Banegas, Jorge E Toblli, Yimin Fang, Feiya Wang, Andrzej Bartke, and Fernando P Dominici

et al . 2011 ). In concordance, genetic deletion of the Mas receptor impairs heart function and induces a profibrotic state ( Santos et al . 2013 ). Consistent with this evidence, the cardiac and renal hypertrophy and fibrosis found in bGH mice were

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Barbara C Fam, Laura J Rose, Rebecca Sgambellone, Zheng Ruan, Joseph Proietto, and Sofianos Andrikopoulos

diabetes. In fact, these mice are growth retarded, have significant cardiac hypertrophy, reduced body weight and adiposity levels and are less sensitive to insulin action ( Katz et al . 1995 ). Studies using ex vivo muscle tissue from these mice have