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2017 ; 3
(3
): 85-97
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Genetics of Magnesium Disorders
#MMPMID29344503
Li H
; Sun S
; Chen J
; Xu G
; Wang H
; Qian Q
Kidney Dis (Basel)
2017[Dec]; 3
(3
): 85-97
PMID29344503
show ga
BACKGROUND: Magnesium (Mg(2+)), the second most abundant cation in the cell, is
woven into a multitude of cellular functions. Dysmagnesemia is associated with
multiple diseases and, when severe, can be life-threatening. SUMMARY: This review
discusses Mg(2+) homeostasis and function with specific focus on renal Mg(2+)
handling. Intrarenal channels and transporters related to Mg(2+) absorption are
discussed. Unraveling the rare genetic diseases with manifestations of
dysmagnesemia has greatly increased our understanding of the complex and
intricate regulatory network in the kidney, specifically, functions of tight
junction proteins including claudin-14, -16, -19, and -10; apical ion channels
including: TRPM6, K(v)1.1, and ROMK; small regulatory proteins including AC3 and
ANK3; and basolateral proteins including EGF receptor, ?-subunit (FXYD2) of
Na-K-ATPase, K(ir)4.1, CaSR, CNNM2, and SLC41A. Although our understanding of
Mg(2+) handling of the kidney has expanded considerably in the last two decades,
many questions remain. Future studies are needed to elucidate a multitude of
unknown aspects of Mg(2+) handling in the kidney. KEY MESSAGE: Understanding rare
and genetic diseases of Mg(2+) dysregulation has expanded our knowledge and
furthers the development of strategies for preventing and managing dysmagnesemia.