Omic studies reveal the pathogenic lipid droplet proteins in non-alcoholic fatty liver disease

被引:30
作者
Zhang, Xuelin [1 ]
Wang, Yang [2 ]
Liu, Pingsheng [2 ]
机构
[1] Capital Univ Phys Educ & Sports, Sch Kinesiol & Hlth, Beijing 100191, Peoples R China
[2] Chinese Acad Sci, Ctr Excellence Biomacromol, Inst Biophys, Natl Lab Biomacromol, Beijing 100101, Peoples R China
基金
中国国家自然科学基金;
关键词
non-alcoholic fatty liver disease; lipid droplets; genome-wide association study; proteomics; PNPLA3; 17; beta-HSD13; GENOME-WIDE ASSOCIATION; 17-BETA-HYDROXYSTEROID DEHYDROGENASES; CARDIOVASCULAR-DISEASE; INSULIN-RESISTANCE; HEPATIC STEATOSIS; MOUSE-LIVER; PNPLA3; EXPRESSION; GENE; STEATOHEPATITIS;
D O I
10.1007/s13238-016-0327-9
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Non-alcoholic fatty liver disease (NAFLD) is an epidemic metabolic condition driven by an underlying lipid homeostasis disorder. The lipid droplet (LD), the main organelle involved in neutral lipid storage and hydrolysis, is a potential target for NAFLD therapeutic treatment. In this review, we summarize recent progress elucidating the connections between LD-associated proteins and NAFLD found by genome-wide association studies (GWAS), genomic and proteomic studies. Finally, we discuss a possible mechanism by which the protein 17 beta-hydroxysteroid dehydrogenase 13 (17 beta-HSD13) may promote the development of NAFLD.
引用
收藏
页码:4 / 13
页数:10
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