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