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First published online on November 30, 2006.
 Copyright © 2006 by The Physiological Society
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Received August 14, 2006
Revised September 1, 2006
Accepted after revision November 23, 2006

"TRPpathies"

Kirill Kiselyov1*, Abigail Soyombo2, and Shmuel Muallem3

1 University of Pittsburgh
2 University of Texas Southwestern Medical Center
3 University of Texas South Western Medical Center

* To whom correspondence should be addressed. E-mail: kiselyov{at}pitt.edu.

Several members of the TRP family of ion channels have been implicated in human diseases such as mucolipidosis type IV, autosomal dominant polycystic kidney disease, familial focal segmental glomerulosclerosis, hypomagnesemia, and several forms of cancer. While the pathogenesis of some "TRPpathies", such as hypomagnesemia, appears straightforward (a lack of renal and intestinal Mg2+ absorption results in Mg2+ deficiency), in most cases the causal relationship between dysregulation of ion channels and the corresponding diseases remain obscure. The present review focuses on unanswered questions regarding pathogenesis of several TRPpathies for which clear linkage to mutations in TRP channels has been reported in humans.


Key words: Ion channels • Kidney • Lipolysis




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