Format

Send to

Choose Destination
See comment in PubMed Commons below
World J Gastroenterol. 2014 Feb 21;20(7):1768-76. doi: 10.3748/wjg.v20.i7.1768.

Role of endoplasmic reticulum stress in the pathogenesis of nonalcoholic fatty liver disease.

Author information

1
Xue-Qun Zhang, Cheng-Fu Xu, Chao-Hui Yu, Wei-Xing Chen, You-Ming Li, Department of Gastroenterology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, Zhejiang Province, China.

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:

Endoplasmic reticulum stress; Nonalcoholic fatty liver disease; Nonalcoholic steatohepatitis; Unfolded protein response

PMID:
24587654
PMCID:
PMC3930975
DOI:
10.3748/wjg.v20.i7.1768
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Baishideng Publishing Group Inc. Icon for PubMed Central
    Loading ...
    Support Center