Lipocalin 2 in the pathogenesis of fatty liver disease and nonalcoholic steatohepatitis

被引:7
作者
Asimakopoulou, Anastasia [1 ]
Weiskirchen, Ralf [1 ]
机构
[1] RWTH Univ Hosp Aachen, Inst Mol Pathobiochem Expt Gene Therapy & Clin Ch, Aachen, Germany
关键词
FABP; fatty liver disease; insulin resistance; LCN2; lipocalin; NASH; NF-kappa B; NGAL; OXPAT; perlipin; PLIN5; RBP; GELATINASE-ASSOCIATED LIPOCALIN; RETINOL-BINDING-PROTEIN; HEPATOCELLULAR-CARCINOMA CELLS; EARLY URINARY BIOMARKER; SEVERELY OBESE WOMEN; ACUTE KIDNEY INJURY; ACUTE-PHASE PROTEIN; INSULIN-RESISTANCE; BETA-LACTOGLOBULIN; GENE-EXPRESSION;
D O I
10.2217/CLP.14.65
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
The lipocalins were originally classified as a widespread group of transport proteins for small hydrophobic molecules. Although they only share a limited sequence homology their 3D fold is conserved. This group of proteins has been implicated in a multitude of biological processes that most often become visible during disease formation. Lipocalin 2 (LCN2) serves as a siderocalin and protects against bacterial infections. In the liver, LCN2 expression is upregulated during inflammation and in response to cellular stress evolving protective effects during acute and chronic injury. LCN2 was shown to act as an adipokine in the pathogenesis of nonalcoholic fatty liver disease and in control of brown adipose tissue activation. In a nutritional model of nonalcoholic steatohepatitis, LCN2 was identified as a key factor that controls the expression of the perlipin 5 regulating cellular lipid droplet formation. We here summarize experimental and clinical findings linking LCN2 to fatty liver disease.
引用
收藏
页码:47 / 67
页数:21
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