Abstract
Fibrotic diseases occur in a variety of organs and lead to continuous organ injury, function decline, and even failure. Currently effective treatment options are limited. Galectin-3 (Gal-3) is a pleiotropic lectin that plays an important role in cell proliferation, adhesion, differentiation, angiogenesis, and apoptosis. Accumulating evidence indicates that Gal-3 activates a variety of profibrotic factors, promotes fibroblast proliferation and transformation, and mediates collagen production. Recent studies have defined key roles for Gal-3 in fibrogenesis in diverse organ systems, including liver, kidney, lung, and myocardial. To help set the stage for future research, we review recent advances about the role played by Gal-3 in fibrotic diseases. Herein we discuss the potential profibrotic role of Gal-3, inhibition of which may represent a promising therapeutic strategy against tissue fibrosis.
Footnotes
- Received July 16, 2014.
- Accepted September 4, 2014.
This work was supported by National Science Foundation of China [81274172, 81473267, 30801535, 81072686, 81273526, 81473268]; the Open Project Program of State Key Laboratory of Natural Medicines, China Pharmaceutical University [SKLNMKF201206]; and Traditional Chinese Medicine research project of the health department of Anhui Province [2012zy53].
- Copyright © 2014 by The American Society for Pharmacology and Experimental Therapeutics
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