骨形态发生蛋白7信号转导与纤维化  

Bone morphogenetic protein 7 signaling and fibrosis

作　　者：丁芹[1] 马会慧[1] 杨绍基[1] 

机构地区：[1]中山大学附属第三医院感染科,广州510630

出　　处：《国际流行病学传染病学杂志》2006年第5期324-326,329,共4页International Journal of Epidemiology and Infectious Disease

基　　金：国家自然科学基金(30571665)

摘　　要：纤维化是指由于多种因素损伤器官实质细胞,使其发生坏死,组织内细胞外基质(ECM)异常增多和过度沉积的病理过程。TGF_β1超家族蛋白是目前已知最重要的致纤维化的细胞因子。骨形态发生蛋白(BMPs)能控制细胞增生与分化,BMPs/Smads信号通路能够在多个环节拮抗TGF_β1的致纤维化作用,尤其是其中的骨形态发生蛋白7(BMP7)具有显著的抗纤维化作用。Fibrosis is caused by many factors. These factors cause too much ECM deposit in tela. The TGF-β1 is known as yet to be the most important cytokine to cause fibrosis. BMPs/Smads signaling can rivalry the fibrogenatie activity of TGF-β1. BMP7 has been shown to have anti-fibrosis effect in different renal diseases models, in cultured mesangial cells, lens epithelial cells, mammary ductal epithelial cells, in lung fibrosis and in peritrabeeular fibrosis. BMP-7 may be an effective treatment to fibrosis in the future.

关 键 词：骨形态发生蛋白7 纤维化 转化生长因子-Β1 SMAD 

分 类 号：R68[医药卫生—骨科学]