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.

糖尿病肾病(DN)是指因胰岛素分泌不足或细胞对胰岛素的反应无效而引起的肾脏微血管并发症，是导致终末期肾病的主要原因。目前，可用的疗法只能缓解症状，不能改善糖尿病肾病的预后。对糖尿病动物的研究表明，在 DN 动物模型中，足细胞和肾小管细胞中 SIRT1 的过表达减轻了蛋白尿和肾损伤。Sirt1 在 DKD 中发挥肾脏保护作用，部分是通过参与疾病发病机制的转录因子的脱乙酰化，如 NF-кB、Smad3、FOXO 和 p53。本综述的目的是强调 SIRT1 参与糖尿病肾病发病机制的保护机制。