(Patho)physiological implications of the novel epithelial Ca2+ channels TRPV5 and TRPV6.
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.
Department of Cell Physiology, Nijmegen Center for Molecular Life Sciences, University Medical Center Nijmegen, PO Box 9101, 6500 HB Nijmegen, The Netherlands.
Tom
T
Nijenhuis
Joost G J
JG
Hoenderop
Bernd
B
Nilius
René J M
RJ
Bindels
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000502:physiology*; D004847:Epithelial Cells / Q000502:physiology*; D006801:Humans; D008659:Metabolic Diseases / Q000378:metabolism / Q000503:physiopathology*; D050916:TRPV Cation Channels
D015220:Calcium Channels; D050916:TRPV Cation Channels; C492239:TRPV5 protein, human; C120776:TRPV6 channel; D002118:Calcium