TGF-β参与糖尿病肾病的发生发展的机制研究现状

Research status of mechanism of TGF-βin the development of diabetic nephropathy

糖尿病(DM)是一种以高血糖为主要特征的代谢性疾病。长期高血糖、胰岛素抵抗和血脂紊乱会引起肾脏等部位的微血管病变,从而引发肾脏疾病,称为糖尿病肾病(diabetes nephropathy,DN)。在DN发生发展的过程中,患者的肾脏通常会出现以肾小球硬化、肾小球及肾小管纤维化为主的病理损伤。DN的发病机制十分复杂,目前普遍认为其与代谢紊乱、血流动力学异常、炎症反应、氧化应激和遗传等多个方面的因素相关。而最新研究发现,转化生长因子-β(TGF-β)的高表达在包括DN在内的多种纤维化疾病中起到关键作用。TGF-β可能分别或同时通过Smad蛋白、丝裂原活化蛋白激酶(MAPK)、磷脂酰肌醇激酶3(PI3K)参与的信号转导途径引起肾损伤,参与DN的发生发展。该文就TGF-β参与DN发生发展机制的研究现状加以综述。

Diabetes mellitus(DM)is a kind of metabolic disease characterized by hyperglycemia.Long-term hyperglycemia,insulin resistance and dyslipidemia will cause microvascular lesions in kidney and other tissues,leading to kidney disease.This kind of disease is called diabetic nephropathy(DN).In the process of DN development,the kidneys of patients usually have pathological damage,mainly glomerulosclerosis,glomerular and tubule fibrosis.The pathogenesis of DN is very complicated,and it is generally believed that DN is related to metabolic disorders,hemodynamic abnormalities,inflammatory response,oxidative stress and genetics.However,recent research found that the high expression of transforming growth factor-β(TGF-β)plays a key role in a variety of fibrotic diseases including DN.TGF-βmay be involved in renal injury and DN development through the signal transduction pathways participated by Smad protein,mitogen activated protein kinase(MAPK),phosphatidylinositol 3-kinase 3(PI3 K),respectively or simultaneously.In this paper,the mechanism of TGF-βparticipating in DN was reviewed.