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

Free Radic Biol Med. 2022 May 20:185:67-75. doi: 10.1016/j.freeradbiomed.2022.04.009. Epub 2022 Apr 27.

Abstract

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.

Keywords: Cideb; ER stress; Hepatic steatosis; Inflammation; Oxidative stress.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis Regulatory Proteins* / metabolism
  • Endoplasmic Reticulum Stress*
  • Fatty Liver* / genetics
  • Fatty Liver* / metabolism
  • Inflammation / metabolism
  • Liver / metabolism
  • Oxidative Stress*

Substances

  • Apoptosis Regulatory Proteins