Fig. 5

AMI inhibited the phosphorylation of AKT/mTOR signaling in hypertrophic cardiomyocytes and CHF hearts. (A) AMI-induced downregulated (fold change ≤ 0.7) and upregulated (fold change ≥ 1.3) phosphorylation sites in cardiomyocytes using a phosphorylation-profiling antibody microarray. (B) KEGG pathway analysis of the AMI-induced differential phosphorylation sites in hypertrophic cardiomyocytes. (C) PPI network analysis of the AMI-induced differential phosphorylation sites in hypertrophic cardiomyocytes. (D) Quantification of p-AKT(Ser473) in cardiomyocytes (n = 3). (E) Quantification of p-mTOR(Ser2481) in cardiomyoyctes (n = 3). (F) Representative western blots of p-mTOR(Ser2481), mTOR, p-AKT(Ser473), AKT, and β-actin in cardiomyoyctes. Original blots are presented in Supplementary Fig. 3. (G) Quantification of p-AKT(Ser473) in post-TAC hearts (n = 3). (H) Quantification of p-mTOR(Ser2481) in post-TAC hearts (n = 3). (I) Representative western blots of p-mTOR(Ser2481), mTOR, p-AKT(Ser473), AKT, and β-actin in post-TAC hearts. Original blots are presented in Supplementary Fig. 4. *P < 0.05 and **P < 0.01.