Fibrosis is a major cause of
end-stage renal disease (
ESRD) a progressive loss in renal function that occurs over a period of months or years, is characterized by a decreased capability of the kidneys to excrete
waste products. There is no specific treatment unequivocally shown to slow the worsening of
chronic kidney disease. Plasma levels of CCN2, a fibrogenic agent, is a predictor of
ESRD and mortality in patients with type 1
diabetic nephropathy. CCN3 has been hypothesized to have antagonistic effects to CCN2 both in vitro and in vivo, including in cultured mesangial cells. In a recent study, van Roeyen and colleagues (Am J Pathol in press, 2012) showed that in vivo overexpression of CCN3 in a model of anti-Thy1.1-induced experimental
glomerulonephritis resulted in decreased
albuminuria, glomerulosclerosis and reduced cortical
collagen type I accumulation. CCN3 enhanced angiogenesis yes suppressed mesangial cell proliferation. Thus
CCN3 protein may represent a novel therapeutic approach to help repair glomerular endothelial damage and mesangioproliferative changes and hence prevent
renal failure, glomerulosclerosis and tubulointerstitial
fibrosis.