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血管紧张素Ⅱ对NRK-52E细胞p38丝裂原激活蛋白激酶信号通路的影响

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摘要 血管紧张素Ⅱ(Ang Ⅱ)可能通过核因子(NF)-κB途径促进肾小管上皮细胞分泌单核细胞趋化蛋白1(MCP-1),加重炎症反应,促进肾脏纤维化。
出处 《中华肾脏病杂志》 CAS CSCD 北大核心 2007年第1期55-56,共2页 Chinese Journal of Nephrology
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参考文献6

  • 1Ruperez M,Sanchez-Lopez E,Blanco-Colio LM,et al.The Rho-kinase pathway regulates angiotensin 11-induced renal damage.Kidney Int Suppl,2005,99:S39-45.
  • 2Sakai N,Wada T,Furnichi K,et al.Involvement of extracellular signal-regulated kinase and p38 in human diabetic nephropathy .Am J Kidney Dis,2005,45:54-65.
  • 3Chen X,Liu W,Wang J,et al.STAT1 and STAT3 mediate thrombin-induced expression of tissue inhibitor of metalloproteinase-1 in human glomerular mesangial cells.Kidney Int,2002,13:1377-1382.
  • 4Hironohu I.Pathogenesis of the fibrosis:role of TGFB1 and CTGF.Curr Opion Rheumat,2002,14:681-685.
  • 5Tohlli JE,Cao G,Casas G,Stella L et al.NF-kappaB and chemokine-cytokine expression in renal tubulointerstitium in experimental hyperoxaluria.Role of the renin-angiotensin system.Urol Res,2005,33:358-367.
  • 6Matsuo H,Tamura M,Kabashima N,et al.Prednisolone inhibits hyperosmolarity-induced expression of MCP-1 via NF-kappaB in peritoneal mesothelial cells.Kidney Int,2006,69:736-746.

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