Diabetic nephropathy (DN) is referred to as the microvascular complication of the kidneys
induced by insufficient production of insulin or an ineffective cellular response to insulin,
and is the main cause of end-stage renal disease. Currently, available therapies provide only symptomatic
relief and fail to improve the outcome of diabetic nephropathy. Studies on diabetic animals
had shown overexpression of SIRT1 in both podocytes and renal tubular cells attenuated proteinuria
and kidney injury in the animal model of DN. Sirt1 exerts renoprotective effects in DKD
in part through the deacetylation of transcription factors involved in the disease pathogenesis, such
as NF-кB, Smad3, FOXO and p53. The purpose of this review is to highlight the protective mechanism
of SIRT1 involved in the pathogenesis of diabetic nephropathy.
Keywords: Diabetic nephropathy, SIRT1, inflammation, calorie restriction, acetylation, ESRD.
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