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2016 ; 25
(4
): 308-13
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Claudins and mineral metabolism
#MMPMID27191348
Hou J
Curr Opin Nephrol Hypertens
2016[Jul]; 25
(4
): 308-13
PMID27191348
show ga
PURPOSE OF REVIEW: The tight junction conductance made of the claudin-based
paracellular channel is important in the regulation of calcium and magnesium
reabsorption in the kidney. This review describes recent findings of the
structure, the function, and the physiologic regulation of claudin-14,
claudin-16, and claudin-19 channels that through protein interactions confer
calcium and magnesium permeability to the tight junction. RECENT FINDINGS:
Mutations in two tight junction genes - claudin-16 and claudin-19 - cause the
inherited renal disorder familial hypomagnesemia with hypercalciuria and
nephrocalcinosis. A recent genome-wide association study has identified
claudin-14 as a major risk gene of hypercalciuric nephrolithiasis. The crystal
structure of claudin-19 has recently been resolved allowing the reconstruction of
a claudin assembly model from cis-dimers made of claudin-16 and claudin-19
interaction. MicroRNAs have been identified as novel regulators of the claudin-14
gene. The microRNA-claudin-14 operon is directly regulated by the Ca sensing
receptor gene in response to hypercalcemia. SUMMARY: The paracellular pathway in
the kidney is particularly important for mineral metabolism. Three claudin
proteins - claudin-14, claudin-16, and claudin-19 - contribute to the structure
and function of this paracellular pathway. Genetic mutations and gene expression
changes in these claudins may lead to alteration of the paracellular permeability
to calcium and magnesium, ultimately affecting renal mineral metabolism.
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