Therapeutic effect of CNP on renal osteodystrophy by antagonizing the FGF-23/MAPK pathway
Therapeutic effect of CNP on renal osteodystrophy by antagonizing the FGF-23/MAPK pathway
复制标题
CNP拮抗FGF-23/MAPK通路对肾性骨营养不良的治疗作用
DOI：
10.3109/10799893.2015.1075041
复制
发表时间：
2016-03
期刊：
影响因子：
--
通讯作者：
Qin YH
中科院分区：
文献类型：
--
作者：
Hu P;Huang BY;Xia X;Xuan Q;Hu B;Qin YH
摘要肾性骨病(Rod)在慢性肾脏病(CKD)中发病率较高。因为大多数Rod患者在早期没有症状，骨活检在许多临床环境中仍然不是常规程序；因此，几个生化指标可能有助于确定Rod的存在。C型利钠肽(CNP)被认为是骨形成的正向调节因子。CKD早期尿CNP排泄量和肾脏CNP表达均明显上调，但随着CKD的进展仍呈进行性下降，推测CNP进行性下降可能是Rod发病的部分原因。此外，成纤维细胞生长因子-23是一种骨源性磷酸盐内分泌调节剂。血清成纤维细胞生长因子-23的升高已被认为是慢性肾脏病的一个共同特征，以1，25-二羟基维生素D值下降为代价来维持正常的血磷。由于CNP和成纤维细胞生长因子-23在骨形成中的作用似乎是相互对立的，因此有理由认为在Rod的发展过程中，它们的信号通路是直接相互作用的。CNP和成纤维细胞生长因子-23通过封闭或相互作用的途径发挥作用，这与最近的研究表明CNP下调丝裂原激活的蛋白激酶活性的作用是一致的。该特定节点可能通过激活环鸟苷一磷酸依赖的蛋白激酶II而在RAF-1水平发挥作用。
Abstract Renal osteodystrophy (ROD) is highly prevalent in chronic kidney disease (CKD). Because most patients with ROD are asymptomatic in the early stage and bone biopsy remains not a routine procedure in many clinical settings; therefore, several biochemical parameters may help to identify the existence of ROD. C-type natriuretic peptide (CNP) is considered as a positive regulator of bone formation. Both urinary excretion and renal expression of CNP are markedly up-regulated in the early stages of CKD, whereas they are still progressively declined accompanied by CKD progression, which invites speculation that the progressive decline of CNP may contribute, in part, to the pathogenesis of ROD. In addition, fibroblast growth factor (FGF)-23 is a bone-derived endocrine regulator of phosphate homeostasis. The elevation of serum FGF-23 has been recognized as a common feature in CKD to maintain normophosphatemia at the expense of declining 1,25-dihydroxyvitamin D values. Since the effects of CNP and FGF-23 on bone formation appear to oppose each other, it is reasonable to propose a direct interaction of their signaling pathways during the progression of ROD. CNP and FGF-23 act through a close or reciprocal pathway and are in agreement with recent studies demonstrating a down-regulatory role of the mitogen-activated protein kinase activity by CNP. The specific node may act at the level of RAF-1 through the activation of cyclic guanosine monophosphate-dependent protein kinases II.
登录
查看更多内容
影响因子：
6.2
作者：
Mirza, Majd Ai;Karlsson, Magnus K.;Larsson, Tobias E.
通讯作者：
Larsson, Tobias E.
DOI：
10.1161/hypertensionaha.110.160796
发表时间：
2011-02
期刊：
Hypertension (Dallas, Tex. : 1979)
影响因子：
--
作者：
Sangaralingham SJ;Huntley BK;Martin FL;McKie PM;Bellavia D;Ichiki T;Harders GE;Chen HH;Burnett JC Jr
通讯作者：
Burnett JC Jr
影响因子：
3.7
作者：
Tassano E;Buttgereit J;Bader M;Lerone M;Divizia MT;Bocciardi R;Napoli F;Pala G;Sloan-Béna F;Gimelli S;Gimelli G
通讯作者：
Gimelli G
影响因子：
7.3
作者：
Rangaswami H;Schwappacher R;Marathe N;Zhuang S;Casteel DE;Haas B;Chen Y;Pfeifer A;Kato H;Shattil S;Boss GR;Pilz RB
通讯作者：
Pilz RB
影响因子：
3.7
作者：
Schibler L;Gibbs L;Benoist-Lasselin C;Decraene C;Martinovic J;Loget P;Delezoide AL;Gonzales M;Munnich A;Jais JP;Legeai-Mallet L
通讯作者：
Legeai-Mallet L