In a mouse model of diabetes, aberrant expression of SDF-1 by glomerular podocytes augmented proteinuria and glomerulosclerosis, while the use of a specific inhibitor of SDF-1, NOX-A12, corrected glomerulosclerosis, enhanced the number of podocytes, maintained the peritubular vasculature and delayed the onset of albuminuria 33. This evidence concerns the gene CXCL12 and glomerulosclerosis.