期刊
BIOFACTORS
卷 37, 期 1, 页码 8-16出版社
WILEY
DOI: 10.1002/biof.135
关键词
saturated fatty acids; ER stress; liver injury; NAFLD
资金
- NATIONAL CENTER FOR RESEARCH RESOURCES [K01RR028135] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK047416, R01DK072017, R56DK072017] Funding Source: NIH RePORTER
- OFFICE OF THE DIRECTOR, NATIONAL INSTITUTES OF HEALTH [K01OD010971] Funding Source: NIH RePORTER
- NCRR NIH HHS [K01 RR028135-01, K01 RR028135] Funding Source: Medline
- NIDDK NIH HHS [R01 DK047416, R56 DK072017-05, R01 DK047416-13, R56 DK072017, R01 DK072017, R01 DK072017-05A1] Funding Source: Medline
- NIH HHS [K01 OD010971] Funding Source: Medline
Nonalcoholic fatty liver disease (NAFLD) represents a burgeoning public health concern in westernized nations. The obesity-related disorder is associated with an increased risk of cardiovascular disease, type 2 diabetes and liver failure. Although the underlying pathogenesis of NAFLD is unclear, increasing evidence suggests that excess saturated fatty acids presented to or stored within the liver may play a role in both the development and progression of the disorder. A putative mechanism linking saturated fatty acids to NAFLD may be endoplasmic reticulum (ER) stress. Specifically, excess saturated fatty acids may induce an ER stress response that, if left unabated, can activate stress signaling pathways, cause hepatocyte cell death, and eventually lead to liver dysfunction. In the current review we discuss the involvement of saturated fatty acids in the pathogenesis of NAFLD with particular emphasis on the role of ER stress. (C) 2010 International Union of Biochemistry and Molecular Biology, Inc.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据