期刊文献+

转化生长因子在后发性白内障形成机制中的研究进展 被引量:2

暂未订购
导出
摘要 白内障是世界范围内的主要致盲原因,手术是白内障最主要的治疗方法。早期的临床资料显示,后发性白内障发生率约为41%,通过近年来技术的革新和人工晶状体材质改变,后发性白内障的发生率有所下降,约为20%-25%。因此研究后发性白内障的作用机制,寻求更加有效的防治方法就意义重大。在以往的研究中发现,在后发障的形成过程中,许多细胞因子发挥重要作用,其中的转化生长因子是近年的研究热点,
出处 《中国实验诊断学》 2014年第2期328-331,共4页 Chinese Journal of Laboratory Diagnosis
  • 相关文献

参考文献3

二级参考文献180

  • 1Oft M, Akhurst RJ, Balmain A. Metastasis is driven by sequential elevation of H-ras and Smad2 levels. Nat Cell Biol 2002; 4:487-494.
  • 2Takano S, Kanai F, Jazag A, et al. Smad4 is essential for down-regulation of E-cadherin induced by TGF-β in pancreatic cancer cell line PANC-1. JBiochem 2007; 141:345-351.
  • 3Kaimori A, Potter J, Kaimori JY, et al. Transforming growth factor-β1 induces an epithelial-to-mesenchymal transition state in mouse hepatocytes in vitro. J Biol Chem 2007; 282:22089-22101.
  • 4Bardeesy N, Cheng KH, Berger JH, et al. Smad4 is dispensable for normal pancreas development yet critical in progres- sion and tumor biology of pancreas cancer. Genes Dev 2006; 20:3130-3146.
  • 5Desgrosellier JS, Mundell NA, McDonnell MA, Moses HL, Barnett JV. Activin receptor-like kinase 2 and Smad6 regulate epithelial-mesenchymal transformation during cardiac valve formation. Dev Biol 2005; 280:201-210.
  • 6Armstrong E J, Bischoff J. Heart valve development: endothelial cell signaling and differentiation. Circ Res 2004; 95:459- 470.
  • 7Saika S, Ikeda K, Yamanaka O, et al. Transient adenoviral gene transfer of Smad7 prevents injury-induced epithelialmesenchymal transition of lens epithelium in mice. Lab Invest 2004; 84:1259-1270.
  • 8Xu GP, Li QQ, Cao XX, et al. The fffect of TGF-β1 and SMAD7 gene transfer on the phenotypic changes of rat al- veolar epithelial cells. Cell Mol Biol Lett 2007; 12:457-472.
  • 9Dooley S, Hamzavi J, Ciuclan L, et al. Hepatocyte-specific Smad7 expression attenuates TGF-β-mediated fibrogenesis and protects against liver damage. Gastroenterology 2008; 135:642-659.
  • 10Zavadil J, Bottinger EP. TGF-β and epithelial-to-mesenchy- real transitions. Oncogene 2005; 24:5764-5774.

共引文献249

同被引文献12

引证文献2

二级引证文献2

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部