Glycogen synthase kinase-3β (GSK-3β) is a serine/threonine protein kinase,which takes part not only in glycogen metabolism,but also in cell proliferation,differentiation and apoptosis. GSK-3β is inhibited by growth...Glycogen synthase kinase-3β (GSK-3β) is a serine/threonine protein kinase,which takes part not only in glycogen metabolism,but also in cell proliferation,differentiation and apoptosis. GSK-3β is inhibited by growth factors and hypertrophic stimuli through phosphorylation of its N-terminal end serine (Ser9) residue. It is also activated by phosphorylation of its tyrosine (Tyr216) residue. GSK-3β is profoundly inactivated in mice with hypertrophic cardiomyopathy (HCM) and plays a secondary role in myosin heavy chain mutation. However,the role of GSK-3β in HCM was controversial. Recent studies have demonstrated that the activation of GSK-3β inhibits the myocardial hypertrophy,and is regulated by Wnt/Frizzld and PI3-K/Akt signaling pathways. This article introduces the molecular role of glycogen synthase kinase-3β signaling in myocardial hypertrophy and the different pathways on the activity of glycogen synthase kinase-3β (GSK-3β)展开更多
文摘目的分析糖尿病肾病患者血清糖原合酶激酶-3β(glycogen synthase kinase-3β,GSK-3β)水平与尿微量白蛋白的相关性,以探究GSK-3β与糖尿病肾病发生发展的关系。方法选取2016年2月至2019年11月新乡医学院第一附属医院收治的117例2型糖尿病患者,根据24h尿白蛋白排泄量(urinary albumin excretion,UAE),将其分为尿白蛋白正常组(UAE<30mg/24h)46例、微量白蛋白尿组(30mg/24h≤UAE≤300mg/24h)39例及大量白蛋白尿组(UAE>300mg/24h)32例,另将同期在本院体检的42例健康志愿者作为对照组。收集各组的临床资料,采用免疫比浊法测定尿液中白蛋白含量,采用酶联免疫吸附法检测血清中GSK-3β水平。结果与对照组相比,尿白蛋白正常组、微量白蛋白尿组、大量白蛋白尿组血清GSK-3β水平显著升高(P<0.05);与尿白蛋白正常组相比,微量白蛋白尿组、大量白蛋白尿组血清GSK-3β水平显著升高(P<0.05);与微量白蛋白尿组相比,大量白蛋白尿组血清GSK-3β水平显著升高(P<0.05)。在2型糖尿病患者中,血清GSK-3β水平与糖化血红蛋白、总胆固醇、低密度脂蛋白、甘油三酯、血肌酐、血尿酸、UAE、病程呈正相关(P<0.05),与高密度脂蛋白呈负相关(P<0.05)。多元逐步线性回归分析结果显示,糖化血红蛋白、血肌酐、血尿酸、UAE影响GSK-3β水平的独立危险因素(P<0.05)。结论血清GSK-3β水平与2型糖尿病患者尿微量白蛋白呈正相关,并随糖尿病肾病的发生及疾病严重程度的加重而逐渐升高,临床监测血清GSK-3β水平变化对于早期发现糖尿病肾病具有重要意义。
文摘Glycogen synthase kinase-3β (GSK-3β) is a serine/threonine protein kinase,which takes part not only in glycogen metabolism,but also in cell proliferation,differentiation and apoptosis. GSK-3β is inhibited by growth factors and hypertrophic stimuli through phosphorylation of its N-terminal end serine (Ser9) residue. It is also activated by phosphorylation of its tyrosine (Tyr216) residue. GSK-3β is profoundly inactivated in mice with hypertrophic cardiomyopathy (HCM) and plays a secondary role in myosin heavy chain mutation. However,the role of GSK-3β in HCM was controversial. Recent studies have demonstrated that the activation of GSK-3β inhibits the myocardial hypertrophy,and is regulated by Wnt/Frizzld and PI3-K/Akt signaling pathways. This article introduces the molecular role of glycogen synthase kinase-3β signaling in myocardial hypertrophy and the different pathways on the activity of glycogen synthase kinase-3β (GSK-3β)
