摘要
钙敏感受体（CaSR）主要表达于甲状旁腺细胞和肾小管上皮细胞，它可通过细胞内信号传导通路改变甲状旁腺激素（PTH）的分泌和。肾小管对电解质和水的处理，调节体内钙平衡，同时CaSR也参与了骨重塑的过程。其遗传性的基因异常可引起各种不同的疾病，包括CaSR失活突变引起的良性家族性低尿钙高钙血症和新生儿期重度甲状旁腺功能亢进，激活突变可引起常染色体显性遗传性低钙血症，与原发性甲状旁腺功能亢进的发病也存在一定的联系。这也为CaSR靶向治疗提供了依据。
Calcium-sensing receptor（CaSR） is expressed in human parathyroid cells and renal tubular epithelial cells mainly. CaSR could control parathyroid hormone （PTH） secretion and the renal tubular＇ s handling of the electrolytes and water. This receptor plays a central role in extracellular calcium homeostasis, and involves in the process of bone remodeling. The change of CaSR function, including anti- CaSR antibodies, CasR gene mutations or any part impairment in CaSR signaling pathway, not only results in the imbalance of PTH and calcium homeostasis, but also relates to disorders of bone remodeling and renal tubular＇ s mishandling in the electrolytes and water, which contribute to hyperparathyroidism. It makes possible clinical use of cinaealcet in hyperparathyroidism in theory.
出处
《国际外科学杂志》
2011年第5期339-342,共4页
International Journal of Surgery
