[1] Sheryanna A, Bhangal G, McDaid J, et al. Inhibition of p38 mitogen-activated protein kinase is effective in the treat- ment of experimental crescentic glomerulonephritis and sup- presses monocyte chemoattractant protein-1 but not IL- 1βor IL-6[J]. J Am Soc Nephrol, 2007, 18(4): 1167-1179.
[2] 赵青, 万毅刚, 王朝俊, 等. 慢性肾脏病肾组织炎症信号通路 p38MAPK 的调节机制及中药的干预作用[J]. 中国中药杂志, 2012, 37(12): 1700-1704.
[3] Polzer K, Soleiman A, Baum W, et al. Selective p38MAPK isoform expression and activation in antineutrophil cytoplasmatic antibody-associated crescentic glomerulon- ephritis: role of p38MAPKα[J]. Ann Rheum Dis, 2008, 67 (5): 602-608.
[4] Pengal R, Guess AJ, Agrawal S, et al. Inhibition of the pro- tein kinase MK-2 protects podocytes from nephrotic syn- drome-related injury[J]. Am J Physiol Renal Physiol, 2011, 301(3): F509-F519.
[5] Huber TB, Hartleben B, Winkelmann K, et al. Loss of podocyte aPKCλ/ιcauses polarity defects and nephrotic syndrome[J]. J Am Soc Nephrol, 2009, 20(4): 798-806.
[6] Menne J, Park JK, Boehne M, et al. Diminished loss of proteoglycans and lack of albuminuria in protein kinase C- α-deficient diabetic mice[J]. Diabetes, 2004, 53(8): 2101- 2109.
[7] Tossidou I, Starker G, Kr黦er J, et al. PKC-alpha modulates TGF-βsignaling and impairs podocyte survival[J]. Cell Physiol Biochem, 2009, 24(5-6): 627-634.
[8] Schiffer M, Bitzer M, Roberts IS, et al. Apoptosis in podocytes induced by TGF-βand Smad7[J]. J Clin Invest, 2001, 108(6): 807-816.
[9] Guess AJ, Ayoob R, Chanley M, et al. Crucial roles of the protein kinases MK2 and MK3 in a mouse model of glomerulonephritis[J]. PloS One, 2013, 8(1): e54239.
[10] 肖文珍, 桂定坤, 汪年松. Notch信号通路与足细胞损伤的研究进展[J]. 中华临床医师杂志: 电子版, 2012, 6(15): 4380-4383.
[11] Niranjan T, Bielesz B, Gruenwald A, et al. The Notch path- way in podocytes plays a role in the development of glom- erular disease[J]. Nat Med, 2008, 14(3): 290-298.
[12] Waters AM, Wu MY, Onay T, et al. Ectopic notch activa- tion in developing podocytes causes glomerulosclerosis[J]. J Am Soc Nephrol, 2008, 19(6): 1139-1157.
[13] Waters AM, Wu MY, Huang YW, et al. Notch promotes dynamin-dependent endocytosis of nephrin[J]. J Am Soc Nephrol, 2012, 23(1): 27-35.
[14] Sharma S, Sirina Y, Susztaka K. The story of Notch and chronic kidney disease[J]. Curr Opin Nephrol Hypertens, 2011, 20(1): 56-61.
[15] Jiang HK, Jiang H, Luo G. et al. Interleukin 13 expression before and after pulse treatment with methylprednisolone in children with steroid-responsive nephrotic syndrome[J]. Zhongguo Dang Dai Er Ke Za Zhi, 2007, 9(6): 533-536 .
[16] Lai KW, Wei CL, Tan LK, et al. Overexpression of interleukin-13 induces minimal-change-like nephropathy in rats[J]. J Am Soc Nephrol, 2007, 18(5): 1476-1485.
[17] Corren J, Lemanske RF, Hanania NA, et al. Lebrikizumab treatment in adults with asthma[J]. N Engl J Med, 2011, 365(12): 1088-1098.
[18] Chakrabarti A, Chena W, Varner JD. A review of the mam- malian unfolded protein response[J]. Biotechnol Bioeng, 2011, 108(12): 2777-2793.
[19] Markan S, Kohli HS, Joshi K, et al. Up regulation of the GRP-78 and GADD-153 and down regulation of Bcl-2 pro- teins in primary glomerular diseases: a possible involvement of the ER stress pathway in glomerulonephritis[J]. Mol Cell Biochem, 2009, 324(1-2): 131-138.
[20] Ito N, Nishibori Y, Ito Y, et al. mTORC1 activation triggers the unfolded protein response in podocytes and leads to nephrotic syndrome[J]. Lab Invest, 2011, 91(11): 1584- 1595.
[21] Henderson JM, Alexander MP, Pollak MR. Patients with ACTN4 mutations demonstrate distinctive features of glom- erular injury[J]. J Am Soc Nephrol, 2009, 20(5): 961-968.
[22] Duann P, Datta PK, Pan C, et al. Superoxide dismutase mimetic preserves the glomerular capillary permeability barrier to protein[J]. J Pharmacol Exp Ther, 2006, 316(3): 1249-1254.
[23] Marshall CB, Pippin JW, Krofft RD, et al. Puromycin aminonucleoside induces oxidant-dependent DNA damage in podocytes in vitro and in vivo[J]. Kidney Int, 2006, 70 (11): 1962-1973.
[24] 戴艳, 于青, 徐琦, 等. 表没食子儿茶素没食子酸酯对高糖环境下体外小鼠足细胞活性氧的影响[J]. 中华肾脏病杂志, 2009, 25(1): 31-35.
[25] Kinugasa S, Tojo A, Sakai T, et al. Selective albuminuria via podocyte albumin transport in puromycin nephrotic rats is attenuated by an inhibitor of NADPH oxidase[J]. Kidney Int, 2011, 80(12):1328-1338.
[26] Bruschi M, Candiano G, Ciana LD, et al. Analysis of the oxido-redox status of plasma proteins. Technology advances for clinical applications[J]. J Chromatogr B Analyt Technol Biomed Life Sci, 2011, 879(17-18): 1338-1344.
[27] Matsumura H, Ashida A, Hirano K, et al. Protective effect of radical scavenger edaravone against puromycin nephro- sis[J]. Clin Nephrol, 2006, 66(6): 405-410.
[28] Dryer SE, Reiser J. TRPC6 channels and their binding part- ners in podocytes: role in glomerular filtration and pathophysiology[J]. Am J Physiol Renal Physiol, 2010, 299 (4): F689-F701.
[29] Nijenhuis T, Sloan AJ, Hoenderop JG, et al. Angiotensin II contributes to podocyte injury by increasing TRPC6 ex-pression via an NFAT-mediated positive feedback signaling pathway[J]. Am J Pathol, 2011, 179(4): 1719-1732.
[30] Fan Q, Xing Y, Ding J, et al. Reduction in VEGF protein and phosphorylated nephrin associated with proteinuria in adriamycin nephropathy rats[J]. Nephron Exp Nephrol, 2009, 111(4): e92-e102.
[31] 邹艳红, 李静, 聂磊, 等. 血管内皮生长因子在肾病大鼠中的表达及意义[J]. 黑龙江医药科学, 2011, 34(1): 29-30.
[32] Bailey E, Bottomley MJ, Westwell S, et al. Vascular endot- helial growth factor mRNA expression in minimal change, membranous, and diabetic nephropathy demonstrated by non-isotopic in situ hybridisation[J]. J Clin Pathol, 1999, 52(10): 735-738.
[33] Hohenstein B, Colin M, Foellmer C, et al. Autocrine VEGF- VEGF-R loop on podocytes during glomerulonephritis in humans[J]. Nephrol Dial Transplant, 2010, 25(10): 3170- 3180.
[34] Tumlin JA, Galphin CM, Rovin BH. Advanced diabetic neph- ropathy with nephrotic range proteinuria: a pilot Study of the long-term efficacy of subcutaneous ACTH gel on proteinuria, progression of CKD, and urinary levels of VEGF and MCP-1[J]. J Diabetes Res, 2013, doi: 10.1155/2013/ 489869. Epub 2013 Sep 12.
|