CHAPTER 7: Galectin-3 Involvement in Fibrotic Diseases

Xiaosong Jiang, Natalie J. Torok, Joseph J. Barchi

Research output: Chapter in Book/Report/Conference proceedingChapter


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.

Original languageEnglish (US)
Title of host publicationAnti-fibrotic Drug Discovery
EditorsJehrod Brenneman, Malliga R. Iyer
PublisherRoyal Society of Chemistry
Number of pages26
StatePublished - Jan 1 2020

Publication series

NameRSC Drug Discovery Series
ISSN (Print)2041-3203
ISSN (Electronic)2041-3211

ASJC Scopus subject areas

  • Drug Discovery


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