AMPK-associated signaling to bridge the gap between fuel metabolism and hepatocyte viability

Figure 2 Adenosine monophosphate-activated protein kinase regulation of cell viability. Adenosine monophosphate-activated protein kinase (AMPK) protects cells from oxidative stress-induced H₂O₂ production and mitochondrial dysfunction, which results in part from the inhibitory phosphorylation of glycogen synthase kinase 3β (GSK3β). GSK3β inhibits mitochondrial function through voltage-activated anion channel (VDAC) phosphorylation. AMPK activation contributed to cell survival, whereas the regulatory role of S6 kinase-1 (S6K1) in apoptosis is still unclear. HSC: Hepatic stellate cell; PAR: Proliferator-activated receptor; PKC: Protein kinase C; LKB1: Liver kinase B1; ROS: Reactive oxygen species; ANT: Adenine nucleotide translocator.