title: TRP channels in kidney disease.
abstract: Mammalian TRP channel proteins form six-transmembrane cation-permeable channels that may be grouped into six subfamilies on the basis of amino acid sequence homology (TRPC, TRPV, TRPM, TRPA, TRPP, and TRPML). Recent studies of TRP channels indicate that they are involved in numerous fundamental cell functions and are considered to play an important role in the pathophysiology of many diseases. Many TRPs are expressed in kidney along different parts of the nephron and growing evidence suggest that these channels are involved in hereditary, as well as acquired kidney disorders. TRPC6, TRPM6, and TRPP2 have been implicated in hereditary focal segmental glomerulosclerosis (FSGS), hypomagnesemia with secondary hypocalcemia (HSH), and polycystic kidney disease (PKD), respectively. In addition, the highly Ca(2+)-selective channel, TRPV5, contributes to several acquired mineral (dys)regulation, such as diabetes mellitus (DM), acid-base disorders, diuretics, immunosuppressant agents, and vitamin D analogues-associated Ca(2+) imbalance whereas TRPV4 may function as an osmoreceptor in kidney and participate in the regulation of sodium and water balance. This review presents an overview of the current knowledge concerning the distribution of TRP channels in kidney and their possible roles in renal physiology and kidney diseases.
authors.affiliation: Department of Physiology, 286 Physiology, Nijmegen Centre for Molecular Life Sciences, Radboud University Nijmegen, Medical Centre, P.O. Box 9101, NL-6500HB Nijmegen, The Netherlands.
authors.forename: Yu-Juei
authors.initials: YJ
authors.lastname: Hsu
authors.forename: Joost G J
authors.initials: JG
authors.lastname: Hoenderop
authors.forename: René J M
authors.initials: RJ
authors.lastname: Bindels
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism; D053579:Gitelman Syndrome / Q000235:genetics; D005923:Glomerulosclerosis, Focal Segmental / Q000209:etiology / Q000235:genetics; D006801:Humans; D006996:Hypocalcemia / Q000209:etiology / Q000235:genetics; D007674:Kidney Diseases / Q000209:etiology* / Q000235:genetics / Q000503:physiopathology*; D007679:Kidney Medulla / Q000502:physiology; D008275:Magnesium Deficiency / Q000150:complications / Q000235:genetics; D008954:Models, Biological; D007690:Polycystic Kidney Diseases / Q000209:etiology / Q000235:genetics; D050052:TRPC Cation Channels / Q000235:genetics / Q000502:physiology; D000074287:TRPC6 Cation Channel; D050053:TRPM Cation Channels / Q000235:genetics / Q000502:physiology; D050396:TRPP Cation Channels / Q000378:metabolism; D050916:TRPV Cation Channels / Q000235:genetics / Q000502:physiology; D050051:Transient Receptor Potential Channels / Q000235:genetics / Q000502:physiology*
chemical_list: D002118:Calcium; D050052:TRPC Cation Channels; D000074287:TRPC6 Cation Channel; D050053:TRPM Cation Channels; D050396:TRPP Cation Channels; D050916:TRPV Cation Channels; D050051:Transient Receptor Potential Channels; C117032:TRPC6 protein, human; C459082:TRPM6 protein, human; C416986:TRPV4 protein, human; C492239:TRPV5 protein, human