@inbook{2381ee6de26b42d0891d331e848060ba,
title = "CHAPTER 7: Galectin-3 Involvement in Fibrotic Diseases",
abstract = "A variety of signaling pathways contribute to initiating the pathologies associated with fibrotic disease. Galectins are a group of beta-galactoside-binding proteins that are involved in a host of cellular processes, some of which contribute to fibrosis in different organs. Accumulating evidence indicates that of these, Galectin-3 (Gal-3) is a pathogenic mediator in fibrotic diseases in many different organs. The atypical Gal-3 contains a single carbohydrate recognition domain (CRD) attached to an N-terminal peptide sequence that putatively nucleates the formation of oligomers that can form lattice networks when bound to multiple cellular glycans. Pharmacological or genetic knockdown of Gal-3 has been shown to inhibit fibrosis in several organs, and thus has emerged as a valid therapeutic target. This chapter will review the structure and function of Gal-3 and attempt to validate the important role it plays in fibrosis. In addition, the current state of pharmaceutical discovery of Gal-3 inhibitors will be outlined and discussed in the context of fibrotic disease of the heart, liver, lungs and kidneys. A discussion of the challenges facing future Gal-3 inhibitor development for targeting fibrosis will also be included.",
author = "Xiaosong Jiang and Torok, {Natalie J.} and Barchi, {Joseph J.}",
year = "2020",
month = jan,
day = "1",
doi = "10.1039/9781788015783-00185",
language = "English (US)",
series = "RSC Drug Discovery Series",
publisher = "Royal Society of Chemistry",
number = "73",
pages = "185--210",
editor = "Jehrod Brenneman and Iyer, {Malliga R.}",
booktitle = "Anti-fibrotic Drug Discovery",
address = "United Kingdom",
edition = "73",
}