摘要
血清和糖皮质激素调节蛋白激酶-1(protein kinase regulation of serum and glucocorticoid,SGK1)是一个与丝氨酸-苏氨酸蛋白激酶等第二信使具有极高同源性的蛋白激酶。它作为多种信号转导通路和细胞磷酸化的级联交汇点,参与离子通道调节、细胞增殖、存活的细胞转导。在糖尿病病人中,高糖诱导SGK1活化,SGK1使得上皮钠离子通道(Epithelial sodium channel,ENaC)的表达增加。近些年来各种研究发现ENaC表达于非上皮组织,且对糖尿病血管病变,尤其是糖尿病视网膜病变的发病将发挥一定的作用。ENaC通过肾素-血管紧张素-醛固酮系统(Renin-angiotensin-aldosterone system,RAAS系统)介导,血管内皮NO生成减少,血管功能障碍;NADPH氧化酶功能障碍,参与病理性血管的生成;在高血糖条件下SGK作用于下游转录调控因子核转录因子κB(Nuclear factorκB,NF-κB),使得其在细胞核中含量增加,上调凋亡基因的表达,周细胞的凋亡增加。
Serum and glucocorticoid regulated kinase （SGK）is a serine/threonine protein kinase with high homology to PKB/AKT as a second messenger. It act as a intersection of multiple signal transduction pathways and cellular phosphorylation, participate in the regulation of ion channels, cell proliferation and transduction of survival cell. In diabetics, the activati-on of SGK was induced by high glucose ,while SGK increased the expres- sion of ENaC. The expression of ENaC in renal tubular epithelial cells and other epithelial tissues has been proved, in recent years, various studies have shown that ENaC expressed in vascular endothelial cells, vascular smooth muscle, retinal neurons, photoreceptors and other non epithelial tissue. We inferred that changes in the expression for these non epithelial tissue of ENaC on diabetic vascular disease, especially the incidence of diabetic retinopathy will play a certain role. ENaC enables the reducti-on of vascular endothelial NO production,leading to vascular dysfunC -tion; NADPH oxidase ＇ s dysfunction participates in the generation of pathological vessels;under high glucose conditions, SGK act on the downstream transcription factor nuclear factor KB, resunting the increasing of the content in the nucleus, upregulating the expression of apoptosis gene,leading to apoptosis of pericytes.
出处
《内蒙古医科大学学报》
2017年第2期167-171,178,共6页
Journal of Inner Mongolia Medical University
