【摘 要】
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Objectives:Mechanical stress on the heart can lead to different results.Physiological stimuli such asexercise cause adaptive cardiac hypertrophy, which characterized by a normal cardiac structure and
【机 构】
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State Key Laboratory of Space Medicine Fundamentals and Application, China Astronaut Research and Tr
论文部分内容阅读
Objectives:Mechanical stress on the heart can lead to different results.Physiological stimuli such asexercise cause adaptive cardiac hypertrophy, which characterized by a normal cardiac structure and normal or enhanced cardiacfunction.Pathological stimuli such assustained cardiac pressure overloadcause maladaptive cardiac remodelingand ultimately heart failure.Wepreviously showedcasein kinase-2 interacting protein-1 (CKIP-1) was an inhibitor of cardiac hypertrophy by up-regulating the dephosphorylation of HDAC4 through the recruitment of protein phosphatase 2A.However, the role of CKIP-1 in thephysiological cardiac hypertrophy is unknown.The purpose of this paper was to determinewhether CKIP-lwas also involved in the regulation of physiological cardiac hypertrophy.
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