The Role of Galectin-3 in the Kidneys

Abstract

Galectin-3 is a 32- to 35-kDa member of the galectin family of b-galactoside-binding lectins, which is characterized by a carbohydrate recognition domain. Through its carbohydrate-binding function, it regulates cell growth, differentiation, and inflammation. It also plays a complex, context-dependent role in the kidneys. During development, it promotes nephrogenesis and is strongly expressed in the ureteric bud and its derivatives. An increase in the concentration of galectin-3 has been reported to be associated with fibrosis of the kidneys. Elevated levels of plasma galectin-3 are also associated with increased risks of rapid renal function decline, incident chronic kidney disease, and progressive renal impairment, and also with cardiovascular end points, infection, and all-cause mortality in patients with renal function impairment. This review discusses a general survey on galectin-3 expressions in nephrogenesis, kidney injury animal models, clinical renal diseases, renal transplantation and the potential role of galectin-3 for treatment in kidney disease.

Galectin-3 Blockade Reduces Renal Fibrosis in Two Normotensive Experimental Models of Renal Damage

“…Gal-3 has been linked to the development of renal fibrosis in animal models and it is inversely correlated with estimated glomerular filtration rate in humans [9, 10]. Elevated serum levels of Gal-3 have been associated with a higher risk of incident CKD and renal dysfunction, suggesting that Gal-3 can predict renal damage, years before CKD is detected clinically, facilitating targeted treatment and disease prevention [10]. Modified citrus pectin (MCP) (a complex water soluble indigestible polysaccharide riche in β-galactose) is a Gal-3 inhibitor that blocks the lectin’s activity.…”

Hepatic fibrosis scores and serum biomarkers in pediatric hepatology

“…Many serum biomarkers have been studied in BA. Galectin‐3 (GAL3) has been studied in kidney disease; it binds different carbohydrate moieties of molecules in the extracellular matrix and appears to be actively involved in both the inflammatory and the fibrotic pathways . In a study of 58 BA post KP versus 20 control patients, BA patients had higher GAL‐3 levels (5.1 ± 0.3 versus 3.8 ± 0.4 ng/mL; P = 0.01), and GAL‐3 was markedly elevated in BA patients with jaundice compared with those without (6.4 ± 0.5 versus 4.4 ± 0.3 ng/mL; P = 0.001), suggesting it could be a biomarker of bilirubin clearance following KP .…”

Prognostic biomarkers in acute coronary syndrome

“…Some galectins contain just one CRD (galectins 1, 2, 5, 7, 10, 11, 13, 14, 15), others contain two homologous CRDs in a single polypeptide chain, separated by a linker of up to 70 amino acids, whereas GAL-3 contains a non-lectin N-terminal region (about 120 amino acids) connected to a CRD, often referred to as a chimera-like galectin (13). Firstly discovered in 1976, 15 galectin members have been identified and they have been classified into three subgroups depending on their structural differences and on the number of CRD within their polypeptide chains (14). All the members of this family have been numbered according to their order of discovery (i.e., from GAL-1 to GAL-15).…”