Research progress on signaling pathways in cirrhotic portal hypertension

Figure 1 PI3K-AKT-mTOR signaling pathways in the development of hepatic portal hypertension. PI3K-AKT-mTOR: In vivo, growth factors, mitogens and hormones interact with PI3K, which activates Akt that then activates mTOR. Mammals have two mTOR complexes: mTORC1 and mTORC2. Akt can phosphorylate mTORC1 and then activate p70S6K via phosphorylation to inhibit 4E-BP1. Activated p70S6K promotes the proliferation of HSCs and stimulates both the production of ribosomes and the synthesis of collagen and other extracellular matrix constituents. mTORC1 can inhibit 4E-BP1, promote the splitting of VEGF, and regulate angiogenesis. Akt can inactivate tuberous sclerosis complex 2 and enhance mTOR activity. mTORC2 regulates Akt. Akt: Protein kinase B; ECM: Extracellular matrix; HSC: Hepatic stellate cell; mTOR: Mammalian targets of rapamycin; mTORC: Mammalian targets of rapamycin complex; p70S6K: p70 ribosomal protein S6 Kinase; TSC2: Tuberous sclerosis complex 2; VEGF: Vascular endothelial growth factor; 4E-BP1: 4E-binding protein-1.