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Lichun Zhou, Baohua Ma, and Xiuzhen Han

Introduction The simple definition of cardiac hypertrophy is the enlargement of the heart ( Hou & Kang 2012 ). The enlargement of the heart is closely matched to its functional load and, under normal conditions, is primarily constitutive in

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Kristine M Wadosky, Jessica M Berthiaume, Wei Tang, Makhosi Zungu, Michael A Portman, A Martin Gerdes, and Monte S Willis

(He et al. 2015), whereas MuRF3 inhibited PPARβ activity in vivo by mono-ubiquitination ( Quintana et al. 2015 ). In this study, we identify the cardiac ubiquitin ligase MuRF1 as an inhibitor of T3-induced physiological cardiac hypertrophy in

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Leigh J Ellmers, Nicola J A Scott, Jarkko Piuhola, Nobuyo Maeda, Oliver Smithies, Chris M Frampton, A Mark Richards, and Vicky A Cameron

cell death, but also by cardiac fibroblast proliferation and fibrosis ( Swynghedauw 1999 ). Cardiac hypertrophy occurs when terminally differentiated cardiac myocytes respond to an increase in workload or injury (such as hypertension or myocardial

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A S R Araujo, P Schenkel, A T Enzveiler, T R G Fernandes, W A Partata, S Llesuy, M F M Ribeiro, N Khaper, P K Singal, and A Belló-Klein

Introduction Cardiac hypertrophy is an adaptive response to a variety of stimuli, including volume and pressure overload and neurohormonal activation ( Donatelli et al . 2003 , Hu et al . 2003 ). Although cardiomyocyte growth can be a beneficial

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Jennifer A Chalmers, Shuo-Yen J Lin, Tami A Martino, Sara Arab, Peter Liu, Mansoor Husain, Michael J Sole, and Denise D Belsham

1997 , Charloux et al . 1999 ). In this study, we focused on POMC gene expression in normal murine heart and pressure-overload cardiac hypertrophy. In addition, we extended investigations toward additional neuroendocrine genes expressed in the

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Patricia M Lenhart, Stefan Broselid, Cordelia J Barrick, L M Fredrik Leeb-Lundberg, and Kathleen M Caron

development of cardiac hypertrophy and transition to heart failure ( Barrick et al . 2012 ). For these reasons, we considered that GPR30, or G-protein-coupled estrogen receptor 1, might be a candidate RAMP3-binding GPCR. GPR30 binds E 2 with high affinity

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Zhousheng Jin, Fangfang Xia, Jiaojiao Dong, Tingting Lin, Yaoyao Cai, Jiali Chen, Xixi Chen, Zhenyang Huang, Quanguang Wang, Hongfei Chen, and Junkai Zhang

studies have implicated that glucocorticoid excess mediates cardiac hypertrophy and other CVDs ( Whitehurst et al. 1999 , Muiesan et al. 2003 ). Circulating level of glucocorticoid is an independent risk factor of CVDs ( Guder et al. 2007

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J G Miquet, J F Giani, C S Martinez, M C Muñoz, L González, A I Sotelo, R K Boparai, M M Masternak, A Bartke, F P Dominici, and D Turyn

leads to the development of biventricular concentric cardiac hypertrophy, characterized by myocardial hypertrophy with interstitial fibrosis and lymphomononuclear infiltration. This cardiac pathology is associated with diastolic dysfunction and, if

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Gabriela Placoná Diniz, Ana Paula Cremasco Takano, Erika Bruneto, Francemilson Goulart da Silva, Maria Tereza Nunes, and Maria Luiza Morais Barreto-Chaves

, Dillmann 2009 ). A growing body of evidence indicates that the renin–angiotensin system (RAS) has a critical role in the development of cardiac hypertrophy found in hyperthyroidism and the local RAS, present in the cardiomyocytes, is directly implicated in

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M R Thomas, J P Miell, A M Taylor, R J M Ross, J R Arnao, D E Jewitt, and A M McGregor


Thyroid hormones are essential for the normal growth and development of many tissues. In the rat, hypothyroidism is associated with growth impairment, and hyperthyroidism with the development of a hypercatabolic state and skeletal muscle wasting but, paradoxically, cardiac hypertrophy. The mechanism by which thyroid hormone produces cardiac hypertrophy and myosin isoenzyme changes remains unclear. The role of IGF-I, an anabolic hormone with both paracrine and endocrine actions, in producing cardiac hypertrophy was investigated during this study in hyperthyroid, hypothyroid and control rats. A treated hypothyroid group was also included in order to assess the effect of acute normalization of thyroid function.

Body weight was significantly lower in the hyperthyroid (mean±s.e.m.; 535·5±24·9 g, P<0·05), hypothyroid (245·3±9·8 g, P<0·001) and treated hypothyroid (265·3±9·8 g, P<0·001) animals when compared with controls (618·5±28·6 g). Heart weight/body weight ratios were, however, significantly increased in the hyperthyroid (2·74 ± 0·11×10−3, P<0·01) and treated hypothyroid (2·87±0·07 ×10−3, P<0·001) animals when compared with controls (2·26±0·03 × 10−3). Serum IGF-I concentrations were similar in the control and hyperthyroid rats (0·91±0·07 vs 0·78±0·04 U/ml, P=0·26), but bioactivity was reduced by 70% in hyperthyroid serum, suggesting a circulating inhibitor of IGF. Serum IGF-I levels (0·12±0·03 U/ml, P<0·001) and bioactivity (0·12±0·04 U/ml, P<0·001) were significantly lower in the hypothyroid group. Liver IGF-I mRNA levels were not statistically different in the control and hyperthyroid animals, but were significantly reduced in the hypothyroid animals (P<0·05 vs control). Heart IGF-I mRNA levels were similar in the control and hypothyroid rats, but were significantly increased in the hyperthyroid and treated hypothyroid animals (increased by 32% in hyperthyroidism, P<0·05; increased by 57% in treated hypothyroidism, P<0·01). Cardiac IGF-I was significantly elevated in hyperthyroidism (0·16±0·01 U/mg heart tissue, P<0·01), was low in hypothyroidism (0·08±0·01 U/mg, P<0·01) and was normalized in the treated hypothyroid group (0·11 ± 0·01 U/mg vs control, 0·13±0·01 U/mg).

Low body mass during both hypothyroidism and hyperthyroidism is therefore associated with reduced systemic IGF bioactivity. In hypothyroidism there is a primary defect in the endocrine function of IGF-I, while in hyperthyroidism serum IGF bioactivity is reduced in the presence of normal endocrine production of this anabolic hormone. In contrast, the paracrine actions of IGF-I are increased in the heart during hyperthyroidism, and this hormone appears to play a part in the development of hyperthyroid cardiac hypertrophy.