Suppression of cideb under endoplasmic reticulum stress exacerbated hepatic inflammation by inducing hepatic steatosis and oxidative stress

Previous studies have shown that endoplasmic reticulum (ER) stress contributes to inflammation in several manners. However, whether cell death inducing DFF45-like effector b (Cideb), a lipid droplet (LD) associated protein that plays an important role in hepatic lipid metabolism, participates in this process has not been reported. In the present study, we demonstrated that deficiency of cideb alone did not trigger violent inflammation in the liver. However, the expression of cideb was suppressed by Chop (C/EBP homologous protein) under ER stress, which inhibited the transport of lipoproteins in the liver and led to the exacerbation of hepatic steatosis and oxidative stress, and ultimately exacerbated inflammation. Our results might provide a novel mechanism explaining inflammation triggered by ER stress. [Display omitted] •ER stress inhibited the expression of cideb through Perk-Chop pathway.•The deficiency of cideb aggravated the inflammation triggered by ER stress.•Suppression of cideb by ER stress inhibited the transport of lipoproteins in the liver, which led to hepatic steatosis and oxidative stress.