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

页码：391 / +

页数：3

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