期刊文献+

活性维生素D及其类似物对足细胞的保护作用 被引量:9

Podocytes as target of 1,25-dihydroxyvitamin D_3 and its analogs
下载PDF
导出
摘要 1,25(OH)2D3产生不足是慢性肾脏病(CKD)的主要特征之一,不仅导致钙磷代谢异常及骨矿化障碍,而且加速肾疾病的进展。1,25(OH)2D3及其类似物可减轻CKD患者的蛋白尿,减轻动物模型足细胞的损伤、凋亡和脱落,促进裂孔隔膜蛋白的表达,维持肾小球滤过屏障的完整性。1,25(OH)2D3保护足细胞机制与抑制足细胞肾素-血管紧张素系统、阻断Wnt/β-Catenin和转化生长因子(TGF)-β1信号通路有关。 1, 25 (OH)2D3 deficiency is a prominent feature of chronic kidneydiseases (CKD). It not only leads to abnormalities of calcium and phosphorus metabolism and bone mineralization in CKD patients, but also accelerates the progression of kidney disease. It has been found that 1, 25 (OH)2D3 and its analogs can reduce proteinuria in CKD patients, ameliorate podocyte injury .and loss, promote the expression of slit diaphragm proteins, and maintain the integrity of the glomerualr filtration barrier in animal moders. The mechanisms of 1, 25 (OH)2D3 and its analogs protecting podoeyte involve inhibiting rennin-angiotensin system and blocking Wnt/β-catenin and TGF-β1 signaling pathways in podocytes.
出处 《临床儿科杂志》 CAS CSCD 北大核心 2012年第1期93-96,共4页 Journal of Clinical Pediatrics
关键词 维生素D 足细胞 慢性肾疾病 vitamin D podocyte chronic kidney disease
  • 相关文献

参考文献30

  • 1邹敏书,周建华,余健.一种新的磷调节因子:成纤维细胞生长因子23[J].中华儿科杂志,2010,48(11):875-877. 被引量:4
  • 2García-Canton C,Bosch E,Ramírez A,et al.Vascular calcifi-cation and 25-hydroxyvitamin D levels in non-dialysis patients with chronic kidney disease stages 4 and 5[J].Nephrol Dial Transplant,2011,26(7):2250-2256.
  • 3Drechsler C,Verduijn M,Pilz S,et al.Vitamin D status and clinical outcomes in incident dialysis patients:results from the NECOSAD study[J].Nephrol Dial Transplant,2011,26(3):1024-1032.
  • 4Pilz S,Tomaschitz A,Friedl C,et al.Vitamin D status and mortality in chronic kidney disease[J].Nephrol Dial Transplant,2011,26(11):3603-3609.
  • 5Mehrotra R,Kermah DA,Salusky IB,et al.Chronic kidney disease,hypovitaminosis D,and mortality in the United States[J].Kidney Int,2009,76(9):977-983.
  • 6Stubbs JR,Idiculla A,Slusser J,et al.Cholecalciferol supple-mentation alters calcitriol-responsive monocyte proteins and decreases inflammatory cytokines in ESRD[J].J Am Soc Nephrol,2010,21(2):353-361.
  • 7Agarwal R,Acharya M,Tian J,et al.Antiproteinuric effect of oral paricalcitol in chronic kidney disease[J].Kidney Int,2005,68(6):2823-2828.
  • 8Alborzi P,Patel NA,Peterson C,et al.Paricalcitol reduces albuminuria and inflammation in chronic kidney disease:a randomized double-blind pilot trial[J].Hypertension,2008,52(2):249-255.
  • 9de Zeeuw D,Agarwal R,Amdahl M,et al.Selective vitamin D receptor activation with paricalcitol for reduction of albuminuria in patients with type 2 diabetes (VITAL study):a randomised controlled trial[J].Lancet,2010,376(9752):1543-1551.
  • 10Stumpf WE,Sar M,Reid FA,et al.Target cells for 1,25-dihydroxyvitamin D3 in intestinal tract,stomach,kidney,skin,pituitary,and parathyroid[J].Science,1979,206(4423):1188-1190.

二级参考文献28

  • 1Urakawa I,Yamazaki Y,Shimada T,et al.Klotho converts canonical FGF receptor into a specific receptor for FGF23.Nature,2006,444:770-774.
  • 2Liu S,Quarles LD.How fibroblast growth factor 23 works.J Am Soc Nephrol,2007,18:1637-1647.
  • 3Razzaque MS,Lanske B.The emerging role of the fibroblast growth factor-23-klotho axis in renal regulation of phosphate homeostasis.J Endocrinol,2007,194:1-10.
  • 4Shimada T,Yamazaki Y,Takahashi M,et al.Vitamin D receptor-independent FGF23 actions in regulating phosphate and vitamin D metabolism.Am J Physiol Renal Physiol,2005,289:F1088-1095.
  • 5Kuro-o M.Klotho in chronic kidney disease-what's new? Nephrol Dial Transplant,2009,24:1705-1708.
  • 6Ben-Dov IZ,Galitzer H,Lavi-MoshayoffV,et al.The Parathyroid is a target organ for FGF23 in rats J Clin Invest,2007,117:4003-4008.
  • 7Mirza MA,Hansen T,Johansson L,et al.Relationship between circulating FGF23 and total body atherosclerosis in the community.Nephrol Dial Transplant,2009,24:3125 -3131.
  • 8Gutiérrez OM,Mannstadt M,Isakova T,et al.Fibroblast growth factor 23 and mortality among patients undergoing hemodialysis.N Engl J Med,2008,359:584-592.
  • 9Ketteler M,Biggar PH.As nature did not predict dialysis--what we can learn from FGF23 in end-stage renal disease? Nephrol Dial Transplant,2009,24:2618-2620.
  • 10Nakanishi S,Kazama JJ,Nii-Kono T,et al.Serum fibroblast growth factor-23 levels predict the future refractory hyperparathyroidism in dialysis patients.Kidney Int,2005,67:1171-1178.

共引文献3

同被引文献116

  • 1王凤英,卢思广,赵彤,李国民.系膜增生型原发性肾病综合征患儿细胞毒性T淋巴细胞相关抗原4基因多态性、蛋白表达及外周血淋巴细胞凋亡的研究[J].中华儿科杂志,2007,45(8):633-634. 被引量:5
  • 2Kallui R,Neilson EG. Epithelial-mesenchymal transition and its implications for fibrosis. J Clin Invest,2003,112:1776-1784.
  • 3Matsui I,Hamano T,Tomida K,et al. Active vitamin D and its analogue,22-oxacalcitriol, ameliorate puromycin aminonucleo- side-induced nephrosis in rats. Nephrol Dial Transplant, 2009,24 (8) :2354-2361.
  • 4Hills CE,Siamantouras E,Smith SW,et al. TGF- modulates cell-to-cell communication in early epithelial-to-mesenehymal transition. Diabetologia,2012,55(3) :812-824.
  • 5Hills CE,Squires PE. The role of TGF-13 and epithelial-to-mes- enchymal transition in diabetic nephropathy. Cytokine Growth Factor Rev,2011,22(3) : 131-139.
  • 6Motazed R,Colville-Nash P,Kwan JT,et al. BMP-7 and proximal tubule epithelial cell: activation of multiple signaling pathways reveals a novel anti-fibrotie mechanism. Pharm Res,2008,25 (10) :2440-2446.
  • 7Nguyen TQ,Roestenberg P,Van Neiuwenhoven FA,et al. CTGF inhibits BMP-7 signaling in diabetic nephropathy. J Am Soc Nephrol, 2008,19 ( 11 ) :2098-2107.
  • 8Zeisberg M,Kalluri R. The role of epithelial-to-mesenehymal transition in renal fibrosis. Mol Med,2004,82(3) : 175-181.
  • 9Rodrguez-lturbe B, Garefa-Garcia G. The role of tubulointersti- tial inflammation in the progression of chronic renal failure. Nephron Clin Pract,2010,116(2) :81-88.
  • 10He W, Kang YS, Dai C, et al. Blockade of Wnt/[3-Catenin Signal- ing by pariealeitol Ameliorates Proteinuria and kidney injury. J Am Soe Nephrol, 2011,22( 1 ) : 90-103.

引证文献9

二级引证文献56

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