The osteocyte in CKD: new concepts regarding the role of FGF23 in mineral metabolism and systemic complications.

The osteocyte in CKD: new concepts regarding the role of FGF23 in mineral metabolism and systemic complications.
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DOI:
10.1016/j.bone.2012.10.008
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发表时间:
2013-06
期刊:
影响因子:
4.1
通讯作者:
Jueppner, Harald
Jueppner, Harald
中科院分区:
医学2区
文献类型:
--
作者:
Wesseling-Perry, Katherine;Jueppner, Harald

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慢性肾脏疾病(CKD)患者中骨细胞蛋白成纤维细胞生长因子23 (FGF23)循环水平升高的鉴定,以及最近的数据将这些值与继发性甲状旁腺功能亢进的发病机制和全身性并发症联系起来,改变了肾功能衰竭中骨和矿物质代谢紊乱的病理生理学和治疗方法。现在看来,骨细胞生物学在CKD过程中很早就发生了改变,这些变化对骨生物学以及进行性心血管和肾脏疾病都有影响。由于循环FGF23值受到用于治疗继发性甲状旁腺功能亢进的治疗方法的影响,不同治疗模式对FGF23的影响对矿物质代谢以及发病率和死亡率具有重要意义。需要进一步的研究来确定骨骼矿化和转换异常的初始触发因素,以及当前治疗方案可能对骨细胞生物学产生的潜在影响。
The identification of elevated circulating levels of the osteocytic protein fibroblast growth factor 23 (FGF23) in patients with chronic kidney disease (CKD), along with recent data linking these values to the pathogenesis of secondary hyperparathyroidism and to systemic complications, has changed the approach to the pathophysiology and treatment of disordered bone and mineral metabolism in renal failure. It now appears that osteocyte biology is altered very early in the course of CKD and these changes have implications for bone biology, as well as for progressive cardiovascular and renal disease. Since circulating FGF23 values are influenced by therapies used to treat secondary hyperparathyroidism, the effects of different therapeutic paradigms on FGF23 have important implications for mineral metabolism as well as for morbidity and mortality. Further studies are critically needed to identify the initial trigger for abnormalities of skeletal mineralization and turnover as well as the potential effects that current therapeutic options may have on osteocyte biology.
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