Figure 1: Effect of HDACIs on cell survival in hemorrhagic shock. HDACIs induce phosphorylation of AKT by inhibition of TRB3 and PTEN. While AKT stimulates transcription of cell survival genes through several other pathways, phosphorylated AKT also phosphorylates GSK-3β. Phosphorylated GSK-3β becomes inactivated form, which cannot degrade β-catenin. HDACIs (e.g., VPA) can also directly inhibit GSK-3β. Moreover, HDACIs induce acetylation and nuclear translocation of β-catenin, leading to downstream survival gene transcription. P, phosphorylation; Ac, acetylation.