Search Results

You are looking at 1 - 10 of 102 items for :

  • cardiac hypertrophy x
  • Refine by Access: All content x
Clear All
Free access

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

Free access

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

Introduction The term cardiac remodelling is used to describe the changes in size, shape and function of the heart observed during the development of cardiac disease, and is characterised not only by cardiomyocyte hypertrophy and

Free access

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

Free access

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

Free access

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

Free access

SJ Kaczmarczyk, S Andrikopoulos, J Favaloro, AA Domenighetti, A Dunn, M Ernst, D Grail, M Fodero-Tavoletti, CE Huggins, LM Delbridge, JD Zajac, and J Proietto

The aim of this study was to investigate the metabolic and structural consequences of a decrease in glucose transporter-4 (GLUT4) levels on the heart. The CreLoxP system was utilised to delete GLUT4 in muscle tIssue including heart. The presence of the PGK-neoR cassette in the GLUT4-Lox mice resulted in reduced expression in all tIssues to levels 15-30% of wild-type control mice. In mice expressing Cre recombinase, there was a further reduction of GLUT4 in cardiac tIssue to almost undetectable levels. Cardiac glucose uptake was measured basally and during a euglycaemic/hyperinsulinaemic clamp using 2-deoxy-[1-(14)C]glucose. Insulin-stimulated glucose uptake was normal in hearts expressing 15% of normal GLUT4 levels but markedly reduced in mice with more profound reduction in GLUT4. Cardiac enlargement occurred only when GLUT4 levels were less than 5% of normal values. In heart there is a threshold level of GLUT4 above which insulin-stimulated glucose uptake is maintained. As little as 5% of normal GLUT4 levels expressed in heart is sufficient to prevent the development of cardiac hypertrophy.

Free access

Hong Zhu, Wei Cao, Peng Zhao, Jieyu Wang, Yuying Qian, and Yun Li

suggest that inappropriate activation of cardiac Ang II contributes significantly to the process of cardiac hypertrophy, fibrosis and inflammation ( Snijder et al. 2015 , Ferrario et al. 2016 ). Several signalling molecules have been implicated in the

Free access

Yousheng Xu, Yongshun Wang, Jingjin Liu, Wei Cao, Lili Li, Hongwei Du, Enbo Zhan, Ruoxi Zhang, Huimin Liu, Maoen Xu, Tao Chen, Yilin Qu, and Bo Yu

-0242 . Next, we found HFD increased body weight, but si ATX did not affect the body weight gain ( Fig. 3G ). However, autotaxin deficiency decreased HFD-induced cardiac hypertrophy, exhibited as decreasing values of heart weight/tibia length ( Fig. 3H ), left

Free access

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

Free access

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