Fig. 7: The proposed model of ApoJ/SOAT2 axis in stress-induced hepatosteatosis.

In hepatocytes facing stress, ApoJ mobilizes along with dispersed Golgi to the Golgi–ER contact site, where ApoJ interacts with ER-resident SOAT2 at the N-terminal IDR region and coordinates Chol esterification to produce CE for LD deposition and lipoprotein loading.