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

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Title:	(Patho)physiological implications of the novel epithelial Ca2+ channels TRPV5 and TRPV6.
Author(s):	Nijenhuis, T. ; Hoenderop, J.G.J. ; Nilius, B.; Bindels, R.J.M.
Publication year:	2003
Source:	Pflügers Archiv : European Journal of Physiology, vol. 446, iss. 4, (2003), pp. 401-409
ISSN:	0031-6768
DOI:	https://doi.org/10.1007/s00424-003-1038-7
Publication type:	Article / Letter to editor
Please use this identifier to cite or link to this item : https://hdl.handle.net/2066/187997
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Subject:	UMCN 5.4: Renal disorders
Organization:	Physiology
Journal title:	Pflügers Archiv : European Journal of Physiology
Volume:	vol. 446
Issue:	iss. 4
Page start:	p. 401
Page end:	p. 409
Abstract:	The epithelial Ca(2+) channels TRPV5 and TRPV6 constitute the apical Ca(2+) entry mechanism in active Ca(2+) (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 Ca(2+) 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 Ca(2+) channels.