p44/42MAPK在糖尿病肾病中的研究进展  

Advanced Research of p44/42MAPK in Pathogenesis of Diabetic Nephropathy

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作  者:王玉容[1] 徐勇[1] 

机构地区:[1]泸州医学院附属医院,四川泸州646000

出  处:《医学综述》2010年第14期2084-2086,共3页Medical Recapitulate

基  金:国家自然科学基金(30670980)

摘  要:糖尿病肾病(DN)是与糖尿病相关危及生命的致死性疾病,长期高血糖导致肾小球系膜细胞病理反应,如细胞外基质过度增生并最终导致DN,其发病机制不清。p44/42MAPK信号转导通路可通过巨噬细胞、生长因子介导、纤维连接蛋白表达以及基底膜的破坏参与DN的发病。研究发现,细胞外信号调节激酶p44/42MAPK的阻断剂PD98059可明显延缓DN的发生发展。Diabetic nephropathy is a key factor of fatal renal disease induced by diabetes,long term of high glucose lead to the pathological reaction of glomerular mesangium cell just as extracellular matrix hyperplasy and lead to diabetic nephropathy finally.However,the pathogenesy is not clear.P44 /42MAPK can participate the pathogenesis of diabetic nephropathy by macrophage aggregation,inducing the action of growth factor,expression of fibronectin and destroy the basement memberan.PD98508,Which is the inhibitor of Exracellular signal-regulated kinase p44 /42MAPK can delay the development of diabetic nephropathy.

关 键 词:P44/42MAPK 糖尿病肾病 纤维连接蛋白 

分 类 号:R587.2[医药卫生—内分泌]

 

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