Endoplasmic Reticulum Stress Related Molecular Mechanisms in Nonalcoholic Fatty Liver Disease (NAFLD)

摘要

Non-alcoholic fatty liver disease (NAFLD) is a common public health issue and is considered a main drive for liver diseases. However, the basic mechanisms that trigger the development of NAFLD still remain somewhat elusive. Endoplasmic reticulum (ER) stress facilitates the unfolded protein response (UPR) and contributes to the etiology of steatosis, nonalcoholic steatohepatitis and ultimately hepatocarcinoma. Although ER stress may lead to a cascade of compensatory responses that help to restore ER homeostasis, cell survival and adaptation, prolonged ER stress is known to impose detrimental pathological outcome, involving insulin resistance, ectopic fat deposition, inflammation, apoptosis, and dysregulated autophagy. All of these processes are capable of provoking the onset and development of NAFLD. To this end, it is pertinent to understand the role of ER stress in the onset and progression of NAFLD for proper management of this devastating metabolic disease. Here in this review, we will summarize available information on the recent advances in the potential role for ER stress in the etiology of NAFLD.