The Role of Galectin-3 in Stellate Cell Activation and Liver Fibrosis

被引：0
|
作者：
Jiang, Joy X. [1 ]
Chen, Xiangling [1 ]
Fukada, Hiroo [1 ]
Hsu, Dan K. [2 ]
Liu, Fu-tong [2 ]
Toeroek, Natalie J. [1 ]
机构：
[1] UC Davis Med Ctr, Div Gastroenterol & Hepatol, Dept Internal Med, 4635 2nd Ave,Suite 1001, Sacramento, CA 95817 USA
[2] UC Davis Med Ctr, Dept Dermatol, Sacramento, CA 95817 USA
来源：
GALECTINS AND DISEASE IMPLICATIONS FOR TARGETED THERAPEUTICS | 2012年 / 1115卷
关键词：
GROWTH-FACTOR-BETA; APOPTOTIC BODIES; PHAGOCYTOSIS; PROLIFERATION; MOLECULE; ADHESION; OXIDASE;
D O I：
暂无
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Gal3 (galectin-3) has been known to be involved in the regulation of kidney, lung and liver fibrosis. We have reported a novel mechanism by which Gal3 contributes to fibrogenesis. Extracellular Gal3 is required for tethering of apoptotic bodies by HSC via cross-linking with integrin alpha v beta 3, and consequently promoting HSC activation. On the other hand, phagocytosis induces Gal3 production by both HSC and Kupffer cells. Taken together, Gal3 may become a therapeutic target for antifibrogenic strategy.
引用
收藏
页码：391 / +
页数：3
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