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Podocyte injury with loss of cells into the urine seems to be an early factor in diabetic nephropathy. Advanced glycation end-products (AGEs) are important mediators of structural and functional renal abnormalities in diabetic nephropathy. We and others have previously described that mice with a deletion in the gene for the cell cycle regulatory p27(Kip1) are protected from some features of diabetic nephropathy.

Advanced glycation end-products induce cell cycle arrest and hypertrophy in podocytes