Abstract
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 αvβ3, 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.
| Original language | English (US) |
|---|---|
| Title of host publication | ACS Symposium Series |
| Publisher | American Chemical Society |
| Pages | 391-395 |
| Number of pages | 5 |
| Volume | 1115 |
| ISBN (Print) | 9780841228801 |
| DOIs | |
| State | Published - Dec 18 2012 |
Publication series
| Name | ACS Symposium Series |
|---|---|
| Volume | 1115 |
| ISSN (Print) | 00976156 |
| ISSN (Electronic) | 19475918 |
ASJC Scopus subject areas
- Chemistry(all)
- Chemical Engineering(all)
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Cite this
Jiang, X., Chen, X., Fukada, H., Hsu, D. K., Liu, F-T., & Torok, N. J. (2012). The role of Galectin-3 in stellate cell activation and liver fibrosis. In ACS Symposium Series (Vol. 1115, pp. 391-395). (ACS Symposium Series; Vol. 1115). American Chemical Society. https://doi.org/10.1021/bk-2012-1115.ch023