Endoplasmic Reticulum Stress Inhibition Enhances Liver Tolerance to Ischemia/Reperfusion

C.      Peralta; C.      Brenner

doi:10.2174/092986711795590039

Abstract

In many physiopathological conditions, the cell controls its proper dysfunction via activation of the unfolded protein response to restore efficient protein synthesis and folding in the endoplasmic reticulum. However, whether the aim of unfolded protein response is to promote the cell survival, it can also lead to induction of cell death and then affect the cell fate. Recently, endoplasmic reticulum stress appeared to be critical for acute as well as chronic diseases including neurodegeneration, cardiac disease, cancer, obesity, type 2 diabetes, and ischemia/reperfusion injury. Therefore, inhibition of the endoplasmic reticulum stress could constitute a promising therapeutic strategy to limit cellular damage in pathologies such as hepatic ischemia/reperfusion.

Keywords: Cell death, chemotherapy, endoplasmic reticulum, mitochondrion, unfolded protein response, physiopathological dysfunction, neurodegeneration, cardiac disease