论文部分内容阅读
纤维化是由于各种慢性因素如炎症、免疫、毒素、缺血及血流动力学改变等导致多种器官实质细胞发生坏死,组织内细胞外基质异常增多和过度沉积的病理过程,持续发展可导致器官组织破坏和功能减退。器官纤维化一直是世界医学的研究热点之一,是组织修复过程过度、过强或失控时过量的细胞外间质沉积在组织内引起的。组织修复失调或组织修复过度的原因是局部组织微环境改变,如促纤维化细胞因子表达增加、抑制纤维化细胞因子表达减少、金属基质蛋白酶和(或)金属基质蛋白酶组织抑制剂等表达失衡。转化生长因子β有广泛的生物学作用:调节细胞生长分化、凋亡、迁移、粘附、基质形成以及损伤修复等,在促纤维化作用中是细胞因子中最强的,其中以转化生长因子(transforming growth factor,TGF)-β1最重要。而骨形态发生蛋白(bone morphogenetic protein,BMP)-7具有显著的抗纤维化作用,能够拮抗TGF-β1的促纤维化作用。
Fibrosis is due to a variety of chronic factors such as inflammation, immune, toxins, ischemia and hemodynamic changes lead to necrosis of many kinds of organ parenchymal cells, tissue extracellular matrix abnormalities increased and excessive deposition of the pathological process of sustainable development Causes organ tissue destruction and hypofunction. Organ fibrosis has always been one of the hottest topics in medical research in the world. It is caused by excessive deposition of extracellular interstitial tissue in the tissue when the tissue repair process is over, over or under control. The reason for the abnormal tissue repair or tissue repair is the local tissue microenvironment changes, such as increased expression of pro-fibrotic cytokines, decreased expression of fibrotic cytokines, and imbalanced expression of metal matrix protease and / or metal matrix protease inhibitors. Transforming growth factor β has a wide range of biological effects: regulation of cell growth and differentiation, apoptosis, migration, adhesion, matrix formation and injury repair, in the role of pro-fibrosis is the strongest of cytokines, of which transforming growth factor (transforming growth factor, TGF-β1 most important. Bone morphogenetic protein (BMP) -7 has a significant anti-fibrosis effect and can antagonize the TGF-β1-induced fibrosis.