Li J,Zhang Z,Wang D, et al.Tgf-bctal/smads signaling stimulates renal interstitial fibrosis in experimental aan [J] . J Recept Signal Transduet Res,2009,29:280-285.
[2]
August P,Sharma V,Ding R,Schwartz JE, et al.Transforming growth faetor beta and excess burden of renal disease [J] .Trans Aln Clin Climatol Assoe,2009,120:61-72.
[3]
Matsubara T, Abe H, Arai H, et al. Expression of Smad1 is directly associated with mesangial matrix expansion in rat diabetic nephropathy [J] . Lab Invest. 2006,86(4):357-68.
[4]
Li Q, Feng L, Li J, et al, Urinary Smad1 is a new biomarker for diagnosis and evalu-ating the severity of diabetic nephropathy [J] . Endocrine, 2014,46(1):83-89.
Nangaku M. Mechanisms of tubulointerstitial injury in the kindney: final common Pathways to end-stagerenalfailure [J] . InternMed, 2004, 43(1):9-17.
[7]
Masszi A, Fan L, Rosiv all L, et al. Integrity of cell-cell contacts is a critical regulator of TGF-beta 1-induced epithelial-to-myofibroblast transition: rolefor beta-catenin [J] . Am J Pathol, 2004, 165( 6) : 1955.
[8]
Myint KM, Yamamoto Y, Doi T, et al. RAGE control of diabetic nephropathy in a mouse model: effects o f RAGE gene disruption and administration of low-molecular weight heparin [J] . Diabet es, 2006, 55( 9) : 2510.
[9]
KalluriR, Neilson EC. Epithelial-mesenchymal transition and its implications for fib- rosis [J] .J C lin Invest, 2003, 112: 1776-1784.
[10]
Yang JW, L iu YH. Dissection of key events in tubular epithelial to myofibroblast transition and its implications in renal interstitial fibrosis [J] .Am J Pathol, 2001, 159: 1465 -1475.
