ER stress-induced inflammation: does it aid or impede disease progression?

Trends Mol Med. 2012 Oct;18(10):589-98. doi: 10.1016/j.molmed.2012.06.010. Epub 2012 Aug 8.


Different lines of research have revealed that pathways activated by the endoplasmic reticulum (ER) stress response induce sterile inflammation. When activated, all three sensors of the unfolded protein response (UPR), PERK, IRE1, and ATF6, participate in upregulating inflammatory processes. ER stress in various cells plays an important role in the pathogenesis of several diseases, including obesity, type 2 diabetes, cancer, and intestinal bowel and airway diseases. Moreover, it has been suggested that ER stress-induced inflammation contributes substantially to disease progression. However, this generalization can be challenged at least in the case of cancer. In this review, we emphasize that ER stress can either aid or impede disease progression via inflammatory pathways depending on the cell type, disease stage, and type of ER stressor.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Activating Transcription Factor 6 / genetics
  • Activating Transcription Factor 6 / metabolism
  • Animals
  • Diabetes Mellitus, Type 2 / physiopathology
  • Disease Progression*
  • Endoplasmic Reticulum Stress*
  • Endoribonucleases / genetics
  • Endoribonucleases / metabolism
  • Humans
  • Inflammation / physiopathology*
  • Neoplasms / physiopathology
  • Obesity / physiopathology
  • Pulmonary Disease, Chronic Obstructive / physiopathology
  • Signal Transduction
  • Unfolded Protein Response
  • Up-Regulation
  • eIF-2 Kinase / genetics
  • eIF-2 Kinase / metabolism


  • Activating Transcription Factor 6
  • eIF-2 Kinase
  • Endoribonucleases