期刊
ANNUAL REVIEW OF PHYSIOLOGY, VOL 75
卷 75, 期 -, 页码 479-501出版社
ANNUAL REVIEWS
DOI: 10.1146/annurev-physiol-030212-183705
关键词
tight junction; paracellular; permeability; ion channel; renal tubule; sodium; calcium
类别
资金
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK084059, R01DK062283, P30DK079333] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [U01GM094627] Funding Source: NIH RePORTER
- NIDDK NIH HHS [P30 DK079333, R01 DK084059, R01 DK062283] Funding Source: Medline
- NIGMS NIH HHS [U01 GM094627] Funding Source: Medline
Claudins are tight junction membrane proteins that regulate paracellular permeability of renal epithelia to small ions, solutes, and water. Claudins interact within the cell membrane and between neighboring cells to form tight junction strands and constitute both the paracellular barrier and the pore. The first extracellular domain of claudins is thought to be the pore-lining domain and contains the determinants of charge selectivity. Multiple claudins are expressed in different nephron segments; such differential expression likely determines the permeability properties of each segment. Recent evidence has identified claudin-2 as constituting the cation-reabsorptive pathway in the proximal tubule; claudin-14, -16, and -19 as forming a complex that regulates calcium transport in the thick ascending limb of the loop of Henle; and claudin-4, -7, and -8 as determinants of collecting duct chloride permeability. Mutations in claudin-16 and -19 cause familial hypercalciuric hypomagnesemia with nephrocalcinosis. The roles of other claudins in kidney diseases remain to be fully elucidated.
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