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(Patho)physiological implications of the novel epithelial Ca2+ channels TRPV5 and TRPV6

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Abstract

The epithelial Ca2+ channels TRPV5 and TRPV6 constitute the apical Ca2+ entry mechanism in active Ca2+ (re)absorption. These two members of the superfamily of transient receptor potential (TRP) channels were cloned from the vitamin-D-responsive epithelia of kidney and small intestine and subsequently identified in other tissues such as bone, pancreas and prostate. These channels are regulated by vitamin D as exemplified in animal models of vitamin-D-deficiency rickets. In addition, the epithelial Ca2+ channels might be involved in the multifactorial pathogenesis of disorders ranging from idiopathic hypercalciuria, stone disease and postmenopausal osteoporosis. This review highlights the emerging (patho)physiological implications of these epithelial Ca2+ channels.

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Acknowledgements

This work was supported in part by grants from the Dutch Kidney Foundation (C10.1881), the Dutch Organization of Scientific research (Zon-Mw 016.006.001, Zon-Mw 902.18.298, NWO-ALW 805.09.042 and NWO-ALW 810.38.004), the Belgian Federal Government, the Flemish Government and the Onderzoeksraad KU Leuven (GOA 99/07, F.W.O. G.0237.95, F.W.O. G.0214.99, F.W.O. G. 0136.00, F.W.O. 0172.03) and a grant from the "Alphonse and Jean Forton–Koning Boudewijn Stichting" (R7115 B0).

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Nijenhuis, T., Hoenderop, J.G.J., Nilius, B. et al. (Patho)physiological implications of the novel epithelial Ca2+ channels TRPV5 and TRPV6. Pflugers Arch - Eur J Physiol 446, 401–409 (2003). https://doi.org/10.1007/s00424-003-1038-7

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