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Shi-Yan Li, Cindy X Fang, Nicholas S Aberle II, Bonnie H Ren, Asli F Ceylan-Isik, and Jun Ren

effectively alleviated high glucose-induced p70s6k phosphorylation. GSK-3β is a negative regulator of stress-induced cardiomyocyte hypertrophy and may serve to maintain normal cardiac growth, cell survival and contractile function ( Michael et al

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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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Morag J Young and Amanda J Rickard

of these findings was truly appreciated when inappropriate aldosterone-for-salt status in rodents was shown to produce hypertension, cardiac hypertrophy and fibrosis ( Selye 1946 , Brilla & Weber 1992 ). Large-scale clinical trials have subsequently

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Vincent Ricchiuti, Nathalie Lapointe, Luminita Pojoga, Tham Yao, Loc Tran, Gordon H Williams, and Gail K Adler

of adverse CV events ( Ricchiuti et al . 2009 ). We did not examine the effect of dietary sodium on cardiomyocyte hypertrophy or cardiac fibrosis. Additional studies are needed to determine whether dietary sodium affects these parameters or the

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Vincent Ricchiuti, Christine G Lian, Eveline M Oestreicher, Loc Tran, James R Stone, Tham Yao, Ellen W Seely, Gordon H Williams, and Gail K Adler

. Cardiovascular Research 57 55 – 62 . Bueno OF De Windt LJ Tymitz KM Witt SA Kimball TR Klevitsky R Hewett TE Jones SP Lefer DJ Peng CF 2000 The MEK1-ERK1/2 signaling pathway promotes compensated cardiac hypertrophy in transgenic mice

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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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Pongpan Tanajak, Hiranya Pintana, Natthaphat Siri-Angkul, Juthamas Khamseekaew, Nattayaporn Apaijai, Siriporn C Chattipakorn, and Nipon Chattipakorn

infarction (MI) ( Liu et al . 2012 , 2013 , Joki et al . 2015 ) and cardiac hypertrophy ( Planavila et al . 2013 , 2014 ). Interestingly, an increase in FGF21 levels is associated with future cardiovascular risk in T2DM patients ( Shen et al . 2013

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Yasumasa Ikeda, Ken-ichi Aihara, Sumiko Yoshida, Masashi Akaike, and Toshio Matsumoto

effects against cardiovascular diseases. Many studies have revealed preventive and favorable effects of estrogen on cardiac hypertrophy ( Malhotra et al . 1990 , Weinberg et al . 1999 , van Eickels et al . 2001 , Cavasin et al . 2003 ) and vascular

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Achim Lother, Lisa Deng, Michael Huck, David Fürst, Jessica Kowalski, Jennifer S Esser, Martin Moser, Christoph Bode, and Lutz Hein

al. 2014 , Barrett Mueller et al. 2015 ), promotes inflammation ( Jia et al. 2015 , 2016 , Lother et al. 2016 ) and contributes to cardiac fibrosis and hypertrophy ( Jia et al. 2015 , Lother et al. 2016 ). Cardiac hypertrophy occurs

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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