Role of endoplasmic reticulum stress in the pathogenesis of nonalcoholic fatty liver disease
- 1 January 2014
- journal article
- review article
- Published by Baishideng Publishing Group Inc. in World Journal of Gastroenterology
- Vol. 20 (7), 1768-76
- https://doi.org/10.3748/wjg.v20.i7.1768
Abstract
Nonalcoholic fatty liver disease (NAFLD) has emerged as a common public health problem in recent decades. However, the underlying mechanisms leading to the development of NAFLD are not fully understood. The endoplasmic reticulum (ER) stress response has recently been proposed to play a crucial role in both the development of steatosis and progression to nonalcoholic steatohepatitis. ER stress is activated to regulate protein synthesis and restore homeostatic equilibrium when the cell is stressed due to the accumulation of unfolded or misfolded proteins. However, delayed or insufficient responses to ER stress may turn physiological mechanisms into pathological consequences, including fat accumulation, insulin resistance, inflammation, and apoptosis, all of which play important roles in the pathogenesis of NAFLD. Therefore, understanding the role of ER stress in the pathogenesis of NAFLD has become a topic of intense investigation. This review highlights the recent findings linking ER stress signaling pathways to the pathogenesis of NAFLD.Keywords
This publication has 74 references indexed in Scilit:
- Chromium Alleviates Glucose Intolerance, Insulin Resistance, and Hepatic ER Stress in Obese MiceObesity, 2008
- Activation and Dysregulation of the Unfolded Protein Response in Nonalcoholic Fatty Liver DiseaseGastroenterology, 2008
- CHOP deficiency attenuates cholestasis-induced liver fibrosis by reduction of hepatocyte injuryAmerican Journal of Physiology-Gastrointestinal and Liver Physiology, 2008
- Endoplasmic Reticulum Stress and Liver InjurySeminars in Liver Disease, 2007
- Endoplasmic reticulum stress, hepatocyte CD1d and NKT cell abnormalities in murine fatty liversLaboratory Investigation, 2007
- Endoplasmic reticulum stress induces calcium-dependent permeability transition, mitochondrial outer membrane permeabilization and apoptosisOncogene, 2007
- Signal integration in the endoplasmic reticulum unfolded protein responseNature Reviews Molecular Cell Biology, 2007
- CCAAT/enhancing binding protein β deletion in mice attenuates inflammation, endoplasmic reticulum stress, and lipid accumulation in diet-induced nonalcoholic steatohepatitisJournal of Hepatology, 2007
- The Role of Insulin Resistance in Nonalcoholic Fatty Liver DiseaseJournal of Clinical Endocrinology & Metabolism, 2006
- In vivo assessment of liver cell apoptosis as a novel biomarker of disease severity in nonalcoholic fatty liver diseaseJournal of Hepatology, 2006