The Role Of Melusin/Akt/GSK3β Pathway In Aortic Banding-and Gaq Overexpression-inducing Myocardiac Hypertrophy

PrefaceNowadays, people focus on the early stage of heart failure - "Hypertrophic modulation of left ventricle". The major feature of hypertrophic remodeling is hypertrophy of the cardiomyocytes, which expand in size and increase their protein synthesis. During the past decades, much effort has been focused on deciphering signaling pathways positively mediating cardiac hypertrophy, i. e. MAPK, CaMK/Calcineurin, Pol II and so on. However, the negatively regulating hypertrophy pathway has not been evaluated enough. Accumulating evidence suggests that glycogen synthase kinase - 3β( GSK -3β) negatively regulates cardiac hypertrophy and that the inhibition of GSK - 3β by hypertrophic stimuli is an important mechanism in the stimulation of cardiac hypertrophy. Me-lusin, a novel muscle - specific integrin β1 - interacting protein, has a crucial role in chronic pressure overload hypertrophy, and can blunt the phosphorylation of GSK-3β. Our study aims to elucidate the roles of negative regulating molecules Akt/ GSK - 3β and constructive genes melusin/integrin in cardiac hypertrophic animal models, in order to get some beneficial information to treatment in the future.Material and Methods1. Animal models of aortic banding:40 Wistar rats, male, 80 - 100g, 4 weeks old, were housed under standard...