Role of galectin-3 in autoimmune and non-autoimmune nephropathies.
Galectins are evolutionary conserved β-galactoside binding proteins with a carbohydrate-recognition domain (CRD) of approximately 130 amino acids. In mammals, 15 members of the galectin family have been identified and classified into three subtypes according to CRD organization: prototype, tandem repeat-type and chimera-type galectins. Galectin-3 (gal-3) is the only chimera type galectin in vertebrates containing one CRD linked to an unusual long N-terminal domain which displays non-lectin dependent activities. Although recent studies revealed unique, pleiotropic and context-dependent functions of gal-3 in both extracellular and intracellular space, gal-3 specific pathways and its ligands have not been clearly defined yet. In the kidney gal-3 is involved in later stages of nephrogenesis as well as in renal cell cancer. However, gal-3 has recently been associated with lupus glomerulonephritis, with Familial Mediterranean Fever-induced proteinuria and renal amyloidosis. Gal-3 has been studied in experimental acute kidney damage and in the subsequent regeneration phase as well as in several models of chronic kidney disease, including nephropathies induced by aging, ischemia, hypertension, diabetes, hyperlipidemia, unilateral ureteral obstruction and chronic allograft injury. Because of the pivotal role of gal-3 in the modulation of immune system, wound repair, fibrosis and tumorigenesis, it is not surprising that gal-3 can be an intriguing prognostic biomarker as well as a promising therapeutic target in a great variety of diseases, including chronic kidney disease, chronic heart failure and cardio-renal syndrome. This review summarizes the functions of gal-3 in kidney pathophysiology focusing on the reported role of gal-3 in autoimmune diseases.
Division of Rheumatology, Department of Medicine (DIMED), University of Padova, Italy.
Francesca
F
Saccon
Division of Rheumatology, Department of Medicine (DIMED), University of Padova, Italy.
Mariele
M
Gatto
Division of Rheumatology, Department of Medicine (DIMED), University of Padova, Italy.
Anna
A
Ghirardello
Division of Rheumatology, Department of Medicine (DIMED), University of Padova, Italy.
Luca
L
Iaccarino
Division of Rheumatology, Department of Medicine (DIMED), University of Padova, Italy.
Leonardo
L
Punzi
Division of Rheumatology, Department of Medicine (DIMED), University of Padova, Italy. Electronic address: adoria@unipd.it.
Andrea
A
Doria
D000818:Animals; D059347:Cardio-Renal Syndrome; D005355:Fibrosis; D037502:Galectin 3 / Q000502:physiology*; D006801:Humans; D007668:Kidney / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D008181:Lupus Nephritis; D015398:Signal Transduction
D037502:Galectin 3
Cardio-renal syndrome; Galectin-3; Lupus glomerulonephritis; Renal fibrosis; Renin-angiotensin-aldosterone axis; Systemic lupus erythematosus