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REVIEW ARTICLE
Year : 2018  |  Volume : 3  |  Issue : 2  |  Page : 31-37

Endoplasmic reticulum stress response in nonalcoholic fatty liver disease


1 Department of Biology and Biochemistry, College of Natural Science and Mathematics, University of Houston, Houston, TX 77004, USA
2 Center for Molecular Medicine and Genetics; Department of Biochemistry, Microbiology, and Immunology, Wayne State University School of Medicine, Detroit, MI 48201, USA

Correspondence Address:
Arushana Ali
Department of Biology and Biochemistry, College of Natural Science and Mathematics, University of Houston, Houston, TX 77004
USA
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ed.ed_11_18

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The prevalence of nonalcoholic fatty liver disease (NAFLD) has increased over the past few decades due to a rise in the incidence of Type 2 diabetes and obesity. Sedentary lifestyle coupled with exorbitant consumption of high-caloric diet has been associated with root cause of the epidemic increase in chronic liver diseases. NAFLD is a chronic liver disease which encompasses a spectrum of conditions ranging from simple steatosis to nonalcoholic steatohepatitis (NASH), further leading to irreversible liver cirrhosis. A “multiple hit working model” is a recognized theory that explains the development and progression of NASH, the advanced stage of NAFLD. According to this model, initial hit leads to the development of steatosis, which makes the liver vulnerable to following hits induced by inflammatory cytokines, endotoxins, lipid peroxidation, oxidative stress, endoplasmic reticulum (ER) stress, saturated fatty acid deposition, and/or hepatic organelle dysfunction. These hits eventually result in hepatic fibrosis, inflammation, and apoptosis, which are considered the key features of NASH. Accumulation of hepatic fats leads to the activation of various pathways, including unfolded protein response, which is associated with intracellular stress and inflammation. ER plays a crucial role in restoring cellular homeostasis by directing either through the refolding of misfolded proteins or employing several alternative mechanisms such as ER-associated degradation. ER stress response also causes insulin resistance and inflammation and in the worst cases, culminates in severe liver damage and hepatic cell death, all of which are central to the pathogenesis of NASH. This review sheds some light on recent findings of ER stress response and oxidative stress in the progression of NAFLD.


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