ER-ASSOCIATED PROTEIN DEGRADATION AS A POTENTIAL ANTI-FIBROTIC TARGET IN HEPATIC STELLATE CELLS
<div><p><b>Background: </b>Liver injury activates hepatic stellate cells (HSCs) which drive fibrosis through secreting extracellular matrix proteins. Proteins destined for secretion are cotranslationally translocated into the endoplasmic reticulum (ER), folded, and exported for secretion. Activated HSCs exhibit increased protein translation leading to ER stress, which is sensed by ER membrane proteins Activating transcription factor 6 (ATF6α), Inositol-requiring enzyme 1 (IRE1α), and Protein kinase R-like ER kinase (PERK).