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Multiple integrins have been implicated in modulating renal function. Modulation of integrin function can lead to pathophysiological processes associated with diabetic nephropathy such as alterations in the glomerular filtration barrier and kidney fibrosis. The complexity of these pathophysiological changes implies that multiple integrin subtypes might need to be targeted to ameliorate the progression of renal disease. To address this hypothesis, we investigated the effects of  MK ‐0429, a compound that was originally developed as an  α v β 3 inhibitor for the treatment of osteoporosis, on renal function and fibrosis. We demonstrated that  MK ‐0429 is an equipotent pan‐inhibitor of multiple  av  integrins.  MK ‐0429 dose‐dependently inhibited podocyte motility and also suppressed  TGF ‐ β ‐induced fibrosis marker gene expression in kidney fibroblasts. Moreover, in the obese  ZSF 1 rat model of diabetic nephropathy, chronic treatment with  MK ‐0429 resulted in significant reduction in proteinuria, kidney fibrosis, and collagen accumulation. In summary, our results suggest that inhibition of multiple integrin subtypes might lead to meaningful impact on proteinuria and renal fibrosis in diabetic nephropathy.

An integrin antagonist ( MK ‐0429) decreases proteinuria and renal fibrosis in the ZSF 1 rat diabetic nephropathy model