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在 CKD 患者中,增生甲状旁腺组织中 FGF23 信号通路的下调是否有助于难治性继发性甲状旁腺功能亢进症的发生?

Does the downregulation of the FGF23 signaling pathway in hyperplastic parathyroid glands contribute to refractory secondary hyperparathyroidism in CKD patients?

机构信息

Université de Lyon, Institut National de la Santé et de la Recherche Medical (INSERM) 890, CHU, Saint-Etienne, France.

出版信息

Kidney Int. 2010 Mar;77(5):390-2. doi: 10.1038/ki.2009.512.

DOI:10.1038/ki.2009.512
PMID:20150940
Abstract

Compared to normal tissue, hyperplastic parathyroid glands of patients with chronic kidney disease on dialysis express lower levels of FGFR1 and Klotho proteins. Similar findings are reported in uremic rats with advanced chronic kidney disease. Moreover, in these animals, FGF23 administration fails to reduce PTH serum levels in vivo and to transmit downstream signals in parathyroid cells ex vivo. These findings may explain, at least partly, the concomitant elevation of both FGF23 and PTH serum levels in chronic kidney disease secondary hyperparathyroidism.

摘要

与正常组织相比,接受透析治疗的慢性肾脏病患者的甲状旁腺增生组织表达较低水平的 FGFR1 和 Klotho 蛋白。在患有晚期慢性肾脏病的尿毒症大鼠中也有类似的发现。此外,在这些动物中,FGF23 给药既不能降低体内 PTH 血清水平,也不能传递甲状旁腺细胞的下游信号。这些发现至少可以部分解释继发性甲状旁腺功能亢进症中 FGF23 和 PTH 血清水平同时升高的原因。

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Does the downregulation of the FGF23 signaling pathway in hyperplastic parathyroid glands contribute to refractory secondary hyperparathyroidism in CKD patients?在 CKD 患者中,增生甲状旁腺组织中 FGF23 信号通路的下调是否有助于难治性继发性甲状旁腺功能亢进症的发生?
Kidney Int. 2010 Mar;77(5):390-2. doi: 10.1038/ki.2009.512.
2
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Parathyroid Klotho and FGF-receptor 1 expression decline with renal function in hyperparathyroid patients with chronic kidney disease and kidney transplant recipients.甲状旁腺 Klotho 和 FGF 受体 1 的表达随肾功能下降在慢性肾脏病伴甲状旁腺功能亢进患者和肾移植受者中下降。
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