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

T Nijenhuis, JGJ Hoenderop, B Nilius, RJM Bindels - Pflügers Archiv, 2003 - Springer
T Nijenhuis, JGJ Hoenderop, B Nilius, RJM Bindels
Pflügers Archiv, 2003Springer
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 …
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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