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 beta-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.

Automated summary

Gal-3 is a lectin associated with multiple pathophysiology pathways in renal damage and fibrosis. It plays various roles, including signal transduction, cell adhesion, and immunological chemoattractant protein. Clinical studies and animal models have linked Gal-3 to kidney disease, and Gal-3 inhibitors appear to improve renal disease. This review summarizes the latest literature on Gal-3 in renal pathophysiology, from its role as a biomarker to its potential as a therapeutic agent.