Cardiac-Specific PID1 Overexpression Enhances Pressure Overload-Induced Cardiac Hypertrophy in Mice

Background/Aims: PID1 was originally described as an insulin sensitivity relevance protein, which is also highly expressed in heart tissue. However, its function in the heart is still to be elucidated. Thus this study aimed to investigate the role of PID1 in the heart in response to hypertrophic sti...

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Veröffentlicht in:	Cellular Physiology and Biochemistry 2015-01, Vol.35 (5), p.1975-1985
Hauptverfasser:	Liu, Yaoqiu, Shen, Yahui, Zhu, Jingai, Liu, Ming, Li, Xing, Chen, Yumei, Kong, Xiangqing, Song, Guixian, Qian, Lingmei
Format:	Artikel
Sprache:	eng
Schlagworte:	Akt Animals Cardiac hypertrophy Cardiomegaly - diagnostic imaging Cardiomegaly - etiology Cardiomegaly - pathology Carrier Proteins - genetics Carrier Proteins - metabolism Cellular signal transduction Disease Models, Animal Gene expression Genetic aspects Health aspects Heart enlargement Heart Failure - diagnostic imaging Heart Failure - pathology Heart Ventricles - metabolism Heart Ventricles - pathology Humans Male MAPK Mice Mice, Inbred C57BL Mice, Transgenic Mitogen-Activated Protein Kinases - metabolism Myocardium - metabolism Myocardium - pathology Myosin Heavy Chains - genetics Original Paper PID1 Pressure Promoter Regions, Genetic Proto-Oncogene Proteins c-akt - antagonists & inhibitors Proto-Oncogene Proteins c-akt - metabolism Real-Time Polymerase Chain Reaction Signal Transduction Ultrasonography Up-Regulation
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