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- W3007315664 endingPage "210" @default.
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- W3007315664 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." @default.
- W3007315664 created "2020-03-06" @default.
- W3007315664 creator A5014765105 @default.
- W3007315664 creator A5018173206 @default.
- W3007315664 creator A5074737138 @default.
- W3007315664 date "2020-03-03" @default.
- W3007315664 modified "2023-09-24" @default.
- W3007315664 title "Galectin-3 Involvement in Fibrotic Diseases" @default.
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