[1] |
Xie Y, Chen X. Epidemiology, major outcomes, risk factors, prevention and management of chronic kidney disease in China [J]. Am J Nephrol, 2008, 28(1): 1-7.
|
[2] |
Lai KN. Pathogenesis of IgA nephropathy [J]. Nat Rev Nephrol, 2012, 8(5): 275-283.
|
[3] |
Jin KB, Choi HJ, Kim HT, et al. Cytokine array after cyclosporine treatment in rats [J]. Transplant Proc, 2008, 40(8): 2682-2684.
|
[4] |
Liu BC, Zhang L, Lv LL, et al. Application of antibody array technology in the analysis of urinary cytokine profiles in patients with chronic kidney disease [J]. Am J Nephrol, 2006, 26(5): 483-490.
|
[5] |
Schmitz J, Owyang A, Oldham E, et al. IL-33, an interleukin-1-like cytokine that signals via the IL-1 receptor-related protein ST2 and induces T helper type 2-associated cytokines [J]. Immunity, 2005, 23(5): 479-490.
|
[6] |
Kurowska-Stolarska M, Kewin P, Murphy G, et al. IL-33 induces antigen-specific IL-5+ T cells and promotes allergic-induced airway inflammation independent of IL-4 [J]. J Immunol, 2008, 181(7): 4780-4790.
|
[7] |
Palmer G, Talabot-Ayer D, Lamacchia C, et al. Inhibition of interleukin-33 signaling attenuates the severity of experimental arthritis [J]. Arthritis Rheum, 2009, 60(3): 738-749.
|
[8] |
Li D, Guabiraba R, Besnard AG, et al. IL-33 promotes ST2-dependent lung fibrosis by the induction of alternatively activated macrophages and innate lymphoid cells in mice [J]. J Allergy Clin Immunol, 2014, 134(6): 1422-1432.
|
[9] |
Zhang J, Wang Z, Xu Z, et al. The potential role of IL-33 in renal transplant recipients with chronic allograft dysfunction [J]. Ann Transplant, 2016, 21: 611-618.
|
[10] |
Demirtas L, Turkmen K, Kandemir FM, et al. The possible role of interleukin-33 as a new player in the pathogenesis of contrast-induced nephropathy in diabetic rats [J]. Ren Fail, 2016, 38(6): 952-960.
|
[11] |
Yang F, Zhu P, Duan L, et al. IL-33 and kidney disease [J]. Mol Med Rep, 2016, 13(1): 3-8.
|
[12] |
Deffit SN, Blum JS. A central role for HSC70 in regulating antigen trafficking and MHC class II presentation [J]. Mol Immunol, 2015, 68(2Pt A): 85-88.
|
[13] |
Kim SY, Lee HM, Kim KS, et al. Noninvasive biomarker candidates for cadmium-induced nephrotoxicity by 2DE/MALDI-TOF-MS and SILAC/LC-MS proteomic analyses [J]. Toxicol Sci, 2015, 148(1): 167-182.
|
[14] |
Wyatt RJ, Julian BA. Activation of complement in IgA nephropathy [J]. Am J Kidney Dis, 1988, 12(5): 437-442.
|
[15] |
Liu N, Mori N, Iehara N, et al. Soluble fibrin formation in the mesangial area of IgA nephropathy [J]. Clin Exp Nephrol, 2007, 11(1): 71-76.
|
[16] |
Aziz MA, Badary DM, Hussein MR. Renal damage following alloxan-induced diabetes is associated with generation of reactive oxygen species, alterations of p53, TGF-beta1 and extracellular matrix metalloproteinases in rats [J]. Cell Biol Int, 2017, 41(5): 525-533.
|
[17] |
Brany D, Dvorska D, Slavik P, et al. Survivin and gynaecological tumours [J]. Pathol Res Pract, 2017, 213(4): 295-300.
|
[18] |
Musial K, Bargenda A, Zwolinska D. Urine survivin, E-cadherin and matrix metalloproteinases as novel biomarkers in children with chronic kidney disease [J]. Biomarkers, 2015, 20(3): 177-182.
|