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Diabetic kidney disease, one of the most severe complications associated with diabetes, is characterized by albuminuria, glomerulosclerosis and progressive loss of renal function. Loss of TIMP3, an Extracellular matrix-bound protein, is a hallmark of diabetic nephropathy in human and mouse models, suggesting its pivotal role in renal diseases associated to diabetes. There is currently no specific therapy for diabetic nephropathy, and the ability to restore high TIMP3 activity specifically in the kidney may represent a potential therapeutic strategy for the amelioration of renal injury under conditions in which its reduction is directly related to the disease. Increasing evidence shows that diabetic nephropathy is also regulated by epigenetic mechanisms, including noncoding RNA. This review recapitulates the pathological, diagnostic and therapeutic potential roles of TIMP3 and the noncoding RNA (microRNA, long noncoding RNA) related to its expression, in the progression of diabetic nephropathy.

TIMP3 involvement and potentiality in the diagnosis, prognosis and treatment of diabetic nephropathy