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Galectin-3 in Kidney Diseases: From an Old Protein to a New Therapeutic Target

Galectin-3 (Gal-3) is a 30KDa lectin implicated in multiple pathophysiology pathways including renal damage and fibrosis. Gal-3 binds β-galactoside through its carbohydrate-recognition domain. From intra-cellular to extra-cellular localization, Gal-3 has multiple roles including transduction signal...

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Autores principales: Boutin, Louis, Dépret, François, Gayat, Etienne, Legrand, Matthieu, Chadjichristos, Christos E.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8952808/
https://www.ncbi.nlm.nih.gov/pubmed/35328545
http://dx.doi.org/10.3390/ijms23063124
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author Boutin, Louis
Dépret, François
Gayat, Etienne
Legrand, Matthieu
Chadjichristos, Christos E.
author_facet Boutin, Louis
Dépret, François
Gayat, Etienne
Legrand, Matthieu
Chadjichristos, Christos E.
author_sort Boutin, Louis
collection PubMed
description Galectin-3 (Gal-3) is a 30KDa lectin implicated in multiple pathophysiology pathways including renal damage and fibrosis. Gal-3 binds β-galactoside through its carbohydrate-recognition domain. From intra-cellular to extra-cellular localization, Gal-3 has multiple roles including transduction signal pathway, cell-to-cell adhesion, cell to extracellular matrix adhesion, and immunological chemoattractant protein. Moreover, Gal-3 has also been linked to kidney disease in both preclinical models and clinical studies. Gal-3 inhibition appears to improve renal disease in several pathological conditions, thus justifying the development of multiple drug inhibitors. This review aims to summarize the latest literature regarding Gal-3 in renal pathophysiology, from its role as a biomarker to its potential as a therapeutic agent.
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spelling pubmed-89528082022-03-26 Galectin-3 in Kidney Diseases: From an Old Protein to a New Therapeutic Target Boutin, Louis Dépret, François Gayat, Etienne Legrand, Matthieu Chadjichristos, Christos E. Int J Mol Sci Review Galectin-3 (Gal-3) is a 30KDa lectin implicated in multiple pathophysiology pathways including renal damage and fibrosis. Gal-3 binds β-galactoside through its carbohydrate-recognition domain. From intra-cellular to extra-cellular localization, Gal-3 has multiple roles including transduction signal pathway, cell-to-cell adhesion, cell to extracellular matrix adhesion, and immunological chemoattractant protein. Moreover, Gal-3 has also been linked to kidney disease in both preclinical models and clinical studies. Gal-3 inhibition appears to improve renal disease in several pathological conditions, thus justifying the development of multiple drug inhibitors. This review aims to summarize the latest literature regarding Gal-3 in renal pathophysiology, from its role as a biomarker to its potential as a therapeutic agent. MDPI 2022-03-14 /pmc/articles/PMC8952808/ /pubmed/35328545 http://dx.doi.org/10.3390/ijms23063124 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Boutin, Louis
Dépret, François
Gayat, Etienne
Legrand, Matthieu
Chadjichristos, Christos E.
Galectin-3 in Kidney Diseases: From an Old Protein to a New Therapeutic Target
title Galectin-3 in Kidney Diseases: From an Old Protein to a New Therapeutic Target
title_full Galectin-3 in Kidney Diseases: From an Old Protein to a New Therapeutic Target
title_fullStr Galectin-3 in Kidney Diseases: From an Old Protein to a New Therapeutic Target
title_full_unstemmed Galectin-3 in Kidney Diseases: From an Old Protein to a New Therapeutic Target
title_short Galectin-3 in Kidney Diseases: From an Old Protein to a New Therapeutic Target
title_sort galectin-3 in kidney diseases: from an old protein to a new therapeutic target
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8952808/
https://www.ncbi.nlm.nih.gov/pubmed/35328545
http://dx.doi.org/10.3390/ijms23063124
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