Ca2+ is essential for numerous physiological functions in our bodies. Therefore, its homeostasis is finely maintained through the coordination of intestinal absorption, renal reabsorption, and bone resorption. The Ca2+-selective epithelial channels TRPV5 and TRPV6 have been identified, and their physiological roles have been revealed: TRPV5 is important in final renal Ca2+ reabsorption, and TRPV6 has a key role in intestinal Ca2+ absorption. The TRPV5 knockout mice exhibit renal leak hypercalciuria and accordingly upregulate their intestinal TRPV6 expression to compensate for their negative Ca2+ balance. In contrast, despite their severe negative Ca2+ balance, TRPV6-null mice do not display any compensatory mechanism, thus resulting in secondary hyperparathyroidism. These results indicate that the genes for TRPV5 and TRPV6 are differentially regulated in human diseases associated with disturbed Ca2+ balance such as hypercalciuria, osteoporosis, and vitamin D-resistant rickets.

中文翻译：

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健康和疾病中上皮Ca2 +吸收的机制和调节。

Ca2 +对于我们体内的多种生理功能至关重要。因此，通过肠道吸收，肾脏重吸收和骨吸收的协调，可以很好地维持其稳态。已经确定了Ca2 +选择性上皮通道TRPV5和TRPV6，并揭示了它们的生理作用：TRPV5在最终的肾脏Ca2 +重吸收中很重要，TRPV6在肠道Ca2 +吸收中起关键作用。TRPV5基因敲除小鼠表现出肾脏渗漏性高钙尿症，因此上调了肠道TRPV6的表达以补偿其负的Ca2 +平衡。相反，尽管TRPV6无效的小鼠严重的Ca2 +负平衡，却没有任何补偿机制，从而导致继发性甲状旁腺功能亢进。