ER Stress and Autophagy in Obesity and Nonalcoholic Fatty Liver Disease

Abstract

Purpose of review

This review highlights the extent to which dysfunction of the endoplasmic reticulum (ER) and autophagy contribute to the pathogenesis of obesity-associated hepatic steatosis and non-alcoholic fatty liver disease (NAFLD). We addressed the following questions: what is the role of the unfolded protein response (UPR) and autophagy in the liver? What interactions between the UPR and autophagy are present during the progression of obesity-associated NAFLD? What steps within the pathways of the UPR and autophagy could be potential therapeutic targets for the treatment of NAFLD?

Recent Findings

Recent studies indicate that dysfunction in the UPR and autophagy play important roles in the development of NAFLD and its progression to NASH.

Summary

This review critically evaluates the literature investigating the role of the UPR and autophagy in the progression of NAFLD and highlights potential therapeutic targets.

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