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Jorge N Artaza, Suzanne Reisz-Porszasz, Joan S Dow, Robert A Kloner, James Tsao, Shalender Bhasin and Nestor F Gonzalez-Cadavid

). In line with the latter observations, in transgenic mice with cardiac-specific expression of activated Akt, which reduces cardiomyocyte death and induces cardiac hypertrophy, Mst expression in the heart was considerably induced ( Cook et al. 2002

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John M C Connell and Eleanor Davies

balance in epithelial tissue, aldosterone in the cardiovascular system promotes cardiac hypertrophy, fibrosis and abnormal vascular endothelial function. In the CNS, it appears to regulate blood pressure, salt appetite and sympathetic tone

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N N Chattergoon, G D Giraud and K L Thornburg

adult and it is known that a number of cardiac-related genes contain thyroid response elements. Studies in adult animals demonstrate that increased plasma T 3 levels lead to cardiac hypertrophy ( Tang et al. 2005 , Thomas et al. 2005 ). However

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C R Liu, L Y Li, F Shi, X Y Zang, Y M Liu, Y Sun and B H Kan

phenotype of the hyperthyroid rat has features of hyperthyroidism, including slowly increased BW, elevated HR, cardiac hypertrophy, and higher serum FT 3 and FT 4 levels. The phenotype of the hypothyroid rat also has features of CH, such as slow growth

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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

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Vanesa Jiménez-Amilburu, Susanne Jong-Raadsen, Jeroen Bakkers, Herman P Spaink and Rubén Marín-Juez

genes important for cardiac functioning and development was affected. Interestingly, gata4 appeared up-regulated in our data set. Gata4 overexpression has been reported to cause cardiac hypertrophy ( Liang et al . 2001 ). During physiological

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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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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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Elisa Keating, Ana Correia-Branco, João R Araújo, Manuela Meireles, Rita Fernandes, Luísa Guardão, João T Guimarães, Fátima Martel and Conceição Calhau

, indicative of cardiac hypertrophy, in at 3 and 13 months of age in female offspring of dams exposed to HFA. As cardiac hypertrophy is an important feature of diabetic cardiomyopathy (DCM) ( Nunes et al . 2013 ), we speculate that perigestational exposure to

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Jarrad M Scarlett, Darren D Bowe, Xinxia Zhu, Ayesha K Batra, Wilmon F Grant and Daniel L Marks

WT-Sham 0.16±0.01 g, P <0.001; Table 1 ). The HW-to-BW ratio (HW:BW), a well-established index of cardiac hypertrophy, was significantly greater for WT-MI mice compared to WT-Sham mice (WT-MI 13.7±0.54 g versus WT-Sham 6.39±0.17 g, P <0.001; Table