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Seth A Reini, Garima Dutta, Charles E Wood, and Maureen Keller-Wood

. Conversely, it has been demonstrated that large doses of cortisol infused directly into the fetus in late gestation causes left ventricular (LV) hypertrophy along with an increase in fetal arterial pressure and cardiac expression of angiotensinogen mRNA

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Félix Vargas, Isabel Rodríguez-Gómez, Pablo Vargas-Tendero, Eugenio Jimenez, and Mercedes Montiel

established hypertension have not been explained, although they may involve irreversible morphological changes in the vascular wall ( Folkow 1990 ). Cardiac mass Mechanisms underlying cardiac hypertrophy secondary to elevated thyroid hormone levels include a

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Wu Luo, Lan Huang, Jingying Wang, Fei Zhuang, Zheng Xu, Haimin Yin, Yuanyuan Qian, Guang Liang, Chao Zheng, and Yi Wang

. Inhibition of either STAT3 or EGFR was associated with normalization of factors critical to cardiac fibrosis and hypertrophy. Furthermore, inhibition of EGFR–STAT3 axis prevented the development of functional cardiac deficits in diabetic mice. We confirmed

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Fausto Bogazzi, Francesco Raggi, Federica Ultimieri, Dania Russo, Aldo D'Alessio, Antonella Manariti, Sandra Brogioni, Luca Manetti, and Enio Martino

) apoptosis was reduced in the former and increased in the latter ( Bogazzi et al . 2008 a , b ); ii) cardiac hypertrophy was evident, at histology, in transgenic mice aged 6 months but not in younger animals ( Bollano et al . 2000 , Fu et al . 2000

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F Dong, X Zhang, X Yang, L B Esberg, H Yang, Z Zhang, B Culver, and J Ren

each year. Both clinical and experimental data have demonstrated that uncorrected obesity leads to cardiac hypertrophy and compromised ventricular function such as reduced myocardial contractility and diastolic compliance ( Sowers 1998 , Ren et al

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Fausto Bogazzi, Dania Russo, Francesco Raggi, Mohammad Bohlooly-Y, Jan Tornell, Chiara Sardella, Martina Lombardi, Claudio Urbani, Luca Manetti, Sandra Brogioni, and Enio Martino

Introduction Acromegalic cardiomyopathy is characterized by biventricular hypertrophy and diastolic abnormalities and, in the late stage, by systolic dysfunction, eventually leading to cardiac failure ( Colao et al . 2004 , Giustina et al . 2008

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Rui Song, Xiang-Qun Hu, and Lubo Zhang

prematurely from spontaneous cardiovascular disease such as spontaneous cardiac hypertrophy, left ventricular dysfunction and heart failure ( Oakley et al. 2013 ). Cortisol administration directly to the near-term fetal lambs increased heart mass that was

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Daniel Landau, Chen Chayat, Nili Zucker, Eli Golomb, Channa Yagil, Yoram Yagil, and Yael Segev

no evidence for increased cardiac apoptosis. However, we found an increased expression of structural myocardial response genes, namely β-MHC, ANP, and skeletal α-actin, which have long been considered as markers of hypertrophy of the rat heart

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Sivaporn Sivasinprasasn, Siripong Palee, Kenneth Chattipakorn, Thidarat Jaiwongkum, Nattayaporn Apaijai, Wasana Pratchayasakul, Siriporn C Chattipakorn, and Nipon Chattipakorn

more severe cardiac tissue damage and left ventricular dysfunction after myocardial ischemia and reperfusion (I/R) ( Zhai et al. 2000 ). In estrogen-deprived animals undergoing cardiac I/R, cardiac mitochondria were more damaged leading to impaired

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Cristina Mora, Cristina Pintado, Blanca Rubio, Lorena Mazuecos, Virginia López, Alejandro Fernández, Aurora Salamanca, Brenda Bárcena, Teresa Fernández-Agulló, Carmen Arribas, Nilda Gallardo, and Antonio Andrés

hyperleptinemia ( Lee et al. 2004 ). Recent studies have shown that central and/or peripheral leptin infusion is required to reverse cardiac steatosis in obese leptin-deficient ( ob/ob ) mice ( Rame et al. 2011 , Sloan et al. 2011 ), although myocardial TAG