Galectin-3: its role in asthma and potential as an anti-inflammatory target

0
148

Review

Peng GaoJodie L SimpsonJie Zhang and Peter G Gibson
For all author emails, please log on.
Respiratory Research 2013, 14:136  doi:10.1186/1465-9921-14-136

Published: 9 December 2013

Abstract (provisional)

Galectins constitute an evolutionary conserved family that bind to beta-galactosides. Increasing evidence shows that galectins are involved in many fundamental biological processes such as cellular communication, inflammation, differentiation and apoptosis. Changes in galectin-3 (Gal-3) expression are commonly seen in cancer and pre-cancerous conditions, and Gal-3 may be involved in the regulation of diverse cancer cell activities that contribute to tumourigenesis, cancer progression and metastasis. In addition, Gal-3 is a pro-inflammatory regulator in rheumatoid arthritis. Gal-3 has been shown to be involved in many aspects in allergic inflammation, such as eosinophil recruitment, airway remodeling, development of a Th2 phenotype as well as increased expression of inflammatory mediators. In an in vivo model it was shown that bronchoalveolar lavage (BAL) fluid from ovalbumin-challenged mice contained significantly higher levels of Gal-3 compared to control mice. The molecular mechanisms of Gal-3 in human asthma have not been fully elucidated. This review will focus on what is known about the Gal-3 and its role in the pathophysiological mechanisms of asthma to evaluate the potential of Gal-3 as a biomarker and therapeutic target of asthma.

 

The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production.