Endoplasmic Reticulum Stress Response in Non-Alcholic Fatty Liver Disease: Sophisticated Pathways

Abstract

Non-alcoholic fatty liver disease comprises a broad spectrum of fat-associated liver conditions that can result in end-stage liver disease and the need for liver transplantation. The multiparallel hypothesis suggests that steatohepatitis is the result of numerous conditions acting in parallel, including form genetic susceptibility, lipotoxicity, disturbed gut microbiata to mitochondrial dysfunction, and endoplasmic reticulum(ER) stress. The unfolded protein response as the ER stress response is coordinated primarily by ER transmembrane stress transducers which is a defensive response initially activates the cell to recover from stress or adapt to stress. It reduces the secretory protein load, enhances protein folding and increases clearance capacity by promoting autophagy and ER-associated degradation. However, if these attempts fail or the ER stress gets prolonged, it will induce cell death programs to eliminate the stressed cells. In recent years, ER stress response has been identified as a crucial mechanism in steatohepatitis by leading improper lipid biosynthesis, inflammation, and autophagy or apoptosis.