EAAT3 Participates In The Pathological Process Of Cardiac Hypertrophy By Regulating AMPK And Akt/mTOR-mediated Autophagy

Objective: To explore the effect of glutamate transporter(GT)on cardiac hypertrophy and its mechanism.Method: Cardiac mast cell model was established by PE treatment of cardiomyocytes;transfection and knockdown of EAAT3 were performed by lipofection;EAAT3 expression,AMPK phosphorylation,Akt/mTOR phosphorylation and cells were detected by Western blot.Autophagy level;q-RT PCR was used to detect the expression level of Marker in cardiac hypertrophy;the mouse model of cardiac hypertrophy was established by ISO modeling.Results: EAAT3 gene was expressed higher in normal mice;overexpression of EAAT3 prevented the progression of cardiac hypertrophy;autophagy was up-regulated in cardiac hypertrophy model;EAAT3 inhibited autophagy by inhibiting Akt/mTOR pathway to relieve cardiac hypertrophy;EAAT3 Increase myocardial hypertrophy by upregulating AMPK phosphorylation levels.Conclusion: EAAT3 has a protective effect in cardiac hypertrophy.