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Chiung-Kuei Huang, Soo Ok Lee, Eugene Chang, Haiyan Pang, and Chawnshang Chang

cardiac hypertrophy Cardiac hypertrophy is prevalent in a substantial portion of individuals with hypertension ( Devereux et al . 1987 , Kaplinsky 1994 ) and recognized as an independent risk factor for congestive heart failure and sudden cardiac death

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Mario Patrizio, Marco Musumeci, Ambra Piccone, Carla Raggi, Elisabetta Mattei, and Giuseppe Marano

Introduction Pathological cardiac hypertrophy, which occurs in response to hemodynamic overload, myocardial damage, or defects in sarcomeric proteins, is associated with an enhanced risk of ventricular dysfunction and heart failure. Increased

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Sheng-Gao Tang, Xiao-Yu Liu, Ji-Ming Ye, Ting-Ting Hu, Ying-Ying Yang, Ting Han, and Wen Tan

normal saline solvent) was 8 mg/kg/day (twice daily), which optimized by our researches about STVNa on pressure overload induced cardiac hypertrophy (unpublished) and doses previously shown to be neuroprotective in rats ( Hu et al . 2016 ). Additionally

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M Jankowski, D Wang, S Mukaddam-Daher, and J Gutkowska

cardiac hypertrophy is exaggerated, and its resolution remains incomplete after parturition ( Simmons et al. 2002 ). In response to elevated female steroid hormones during gestation, cardiac growth and contractility are modulated profoundly in

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Victor P Bilan, Eman M Salah, Sheldon Bastacky, Huw B Jones, Rachel M Mayers, Bradley Zinker, Simon M Poucher, and Stevan P Tofovic

cardiac hypertrophy (35% increase in heart weight). Notably, direct hypertrophic effects of rosiglitazone through interaction with growth-promoting signaling pathways have been suggested ( Bell & McDermott 2005 , Festuccia et al . 2009 ). Long

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Beatriz S Amorim, Cintia B Ueta, Beatriz C G Freitas, Renata J Nassif, Cecília Helena de Azevedo Gouveia, Marcelo A Christoffolete, Anselmo S Moriscot, Carmen Lucia Lancelloti, Flávia Llimona, Hermes Vieira Barbeiro, Heraldo Possolo de Souza, Sergio Catanozi, Marisa Passarelli, Marcelo S Aoki, Antonio C Bianco, and Miriam O Ribeiro

%), had less total fat content (−∼70%), less total body water (∼15%; Table 2 ), while at the same time exhibited cardiac hypertrophy (∼23%; Table 1 ). Figure 1 Effects of GC-24 on body weight and composition. Rats were placed on a high-fat diet for 4

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Syed Jalal Khundmiri

cardiac myocytes increases intracellular calcium and activates a signaling cascade that involves production of ROS and activation of the EGFR–Src kinase pathway leading to cardiac hypertrophy ( Xie & Askari 2002 , Mohammadi et al . 2003 ). This

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Kook Hwan Kim and Myung-Shik Lee

another study showed FGF21 induction in the liver and adipose tissue but not in the ischemic myocardium of mice ( Liu et al . 2013 ). Importantly, stress-induced cardiac hypertrophy was increased in Fgf21 − / − mice, while exogenous FGF21 administration

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Charlotte van Noord, Wendy M van der Deure, Miriam C J M Sturkenboom, Sabine M J M Straus, Albert Hofman, Theo J Visser, Jan A Kors, Jacqueline C M Witteman, and Bruno H Ch Stricker

, Owecki et al . 2006 ). A potential explanation for an association with prolongation of the QTc interval is an increased activity of cardiac Na + /K + ATPase in thyroid hormone excess, leading to increased intracellular K + with subsequent membrane

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H Kobori, A Ichihara, Y Miyashita, M Hayashi, and T Saruta

It is well known that renal hypertrophy is induced by hyperthyroidism; however, the mechanism is not fully understood. We recently reported that cardiac hypertrophy in hyperthyroidism is mediated by enhanced cardiac expression of renin mRNA. The present study addresses the hypothesis that renal hypertrophy in hyperthyroidism is mediated by amplification of renal expression of renin mRNA. Twenty Sprague-Dawley rats were divided into control (n=5) and hyperthyroid groups by daily intraperitoneal injections of saline vehicle or thyroxine. The hyperthyroid group was subdivided further into hyperthyroid-vehicle (n=5), hyperthyroid-losartan (n=5), and hyperthyroid-nicardipine (n=5) groups by daily intraperitoneal injections of saline vehicle, losartan, or nicardipine. All rats were killed at 4 weeks, and the blood and kidneys were collected. The kidney-to-body weight ratio increased in the hyperthyroid groups (+34%). Radioimmunoassays and reverse transcriptase-polymerase chain reaction revealed increased renal renin (+91%) and angiotensin II (+65%) levels and enhanced renal renin mRNA expression (+113%) in the hyperthyroid groups. Losartan and nicardipine decreased systolic blood pressure to the same extent, but only losartan caused regression of thyroxine-induced renal hypertrophy. These results suggest that thyroid hormone activates the intrarenal renin-angiotensin system via enhancement of renal renin mRNA expression, which then leads to renal hypertrophy.