Fig. 7: The HBP stimulates mTOR signaling.
From: Chronic activation of hexosamine biosynthesis in the heart triggers pathological cardiac remodeling
a Gfat1 overexpression in NRVMs was sufficient to activate mTOR signaling as shown by an increase in S6 phosphorylation, a downstream event of the mTOR pathway. N = 10 for Ad-GFP; n = 9 for Ad-Gfat1. Student’s t test (two-tailed) was conducted. b Gfat1 overexpression in the heart led to activation of the mTOR pathway. Gfat1 expression was turned on in the double transgenic mice for 2 weeks. After TAC, the heart was harvested to assess mTOR signaling. Pressure overload caused upregulation of S6 phosphorylation that was further potentiated by Gfat1 overexpression. N = 8 for ctrl/sham; n = 9 for other groups. c Gfat1 silencing in NRVMs diminished the mTOR pathway after PE treatment. N = 6 for ctrl si/veh; n = 9 for Gfat1 si/veh; n = 7 for ctrl si/PE; n = 9 for Gfat1 si/PE. d Cardiac-specific knockout of Gfat1 led to a decrease in the mTOR signaling, as evidenced by reduction in S6 phosphorylation. N = 6 for sham; n = 5 for TAC. Data are shown as mean ± SEM. Significance was calculated by two-way ANOVA, followed by Tukey’s test. ***p < 0.001. Source data are provided as a Source Data file.
