蛋白激酶C-β与糖尿病肾病研究的进展  

Advances of protein kinase C beta and diabetic nephropathy

作　　者：赵明明[1] 刘丽梅[1] 

机构地区：[1]上海交通大学附属第六人民医院内分泌代谢科上海市糖尿病研究所,上海200233

出　　处：《上海交通大学学报（医学版）》2014年第4期551-555,共5页Journal of Shanghai Jiao tong University:Medical Science

基　　金：国家自然科学基金(81270876;30771022;30971384);上海市科委优秀学科带头人基金(10XD1403400)~~

摘　　要：PRKCB1基因编码的蛋白激酶C(PKC)-βⅠ和PKC-βⅡ两种亚型,通过PKC信号通路途径在糖尿病肾病的发生和进展中起着重要作用。PKC-β抑制剂通过降低肾小球基膜的厚度和减少微量白蛋白尿,对糖尿病患者的肾脏起着保护作用。PRKCB1基因的多态或变异通过影响该基因的转录活性、增加胰岛素抵抗、促进血管内皮氧化应激,而与糖尿病肾病风险增加及终末期肾病相关。该文就PKC-β与糖尿病肾病关系的研究进展进行综述。Two isoforms of protein kinase C （PKC）, i.e. PKC-βⅠ and -βⅡ, which are encoded by the PRKCB1 gene, play important roles in the development and progression of diabetic nephropathy through the PKC signaling pathway. PKG-β inhibitor can reduce the thickness of glomerular basement membrane and microalbuminuria to protect the renal functions of diabetes patients. Polymorphisms and variants of PRKCB1 gene are relevant to increasing the risk of diabetic nephropathy and end stage renal disease by affecting its transcriptional activity, increasing insulin resistance, and promoting endothelial oxidative stress. This paper reviews the research progresses on the relationship between PKC-β and diabetic nephropathy.

关 键 词：蛋白激酶C-β 糖尿病肾病 PRKCB1基因 

分 类 号：R587.2[医药卫生—内分泌] R692[医药卫生—内科学]