成纤维细胞生长因子23对磷代谢的调控及其临床意义  

The regulation of FGF23 in phosphate homeostasis and its clinical significance

作　　者：陈亚希[1] 张坤[1] 田浩明[1] 余希杰[1] 

机构地区：[1]四川大学华西医院内分泌与代谢病研究室,成都610041

出　　处：《中华骨质疏松和骨矿盐疾病杂志》2012年第3期157-166,共10页Chinese Journal Of Osteoporosis And Bone Mineral Research

基　　金：国家自然科学基金(81072190;30872632);四川省科技厅支撑计划(2010SZ0168);教育部留学回国人员科研启动基金[教外司留(2011)1139号]

摘　　要：成纤维细胞生长因子23(FGF230)是最近发现的一种新型内分泌激素,主要在骨细胞和成骨细胞中表达。FGF23需要与FGFR-α-Klotho复合物结合发挥其生理功能。FGF23通过下调肾脏近曲小管上皮细胞内NPT2a和NPT2c表达降低磷从原尿的重吸收,下调1-羟基酶(Cyp27b1)在肾脏近曲小管的表达降低活性1,25(OH)_2D的合成,进而减少小肠对磷的吸收。磷代谢紊乱常见于先天性代谢疾病和慢性肾病(CKD)。明确FGF23在其中的病理作用将为上述疾病的诊断和治疗提供新思路和目标。Fibroblast growth factor 23 （FGF23） is recently discovered as a new endocrine hormone,predominately produced by osteocytes/osteoblasts. FGF23 exerts its biological functions by interacting with FGFR-α-Klotho complexes. Major functions of FGF23 are to suppress the expressions of NPT2a and NPT2c in the renal proximal tubular cells,thus to increase urinary phosphate excretion. In addition, FGF23 reduces 1,25（OH）2D levels due to the inhibition of 25-hydroxyvitamin D 1-α-hydroxylase（Cyp27b1） and consequently decreases intestinal phosphate absorption. Abnormal phosphate homeostasis can be found in some genetic hyperor hypo-phosphatemia as well as chronic kidney disease（CKD）. This review summarizes recent insights into the regulation of FGF23 on phosphate homeostasis and discusses the involvement of its interactions with some clinical diseases.

关 键 词：磷代谢 成纤维细胞生长因子-23 成纤维细胞生长因子受体 α-Klotho 

分 类 号：R681[医药卫生—骨科学]