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2018 ; 6
(ä): 77
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Novel Aspects of Renal Magnesium Homeostasis
#MMPMID29686978
Giménez-Mascarell P
; Schirrmacher CE
; Martínez-Cruz LA
; Müller D
Front Pediatr
2018[]; 6
(ä): 77
PMID29686978
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Magnesium (Mg(2+)) is indispensable for several vital functions, such as
neurotransmission, cardiac conductance, blood glucose, blood pressure regulation,
and proper function of more than 300 enzymes. Thus, Mg(2+) homeostasis is subject
to tight regulation. Besides the fast and immediate regulation of plasma Mg(2+),
a major part of Mg(2+) homeostasis is realized by a concerted action of
epithelial molecular structures that tightly control intestinal uptake and renal
absorption. This mechanism is provided by a combination of para- and
transcellular pathways. Whereas the first pathway provides the organism with a
maximal amount of vital substances by a minimal energy expenditure, the latter
enables controlling and fine-tuning by means of local and regional regulatory
systems and also, hormonal control. The paracellular pathway is driven by an
electrochemical gradient and realized in principal by the tight junction (TJ), a
supramolecular organization of membrane-bound proteins and their adaptor and
scaffolding proteins. TJ determinants are claudins (CLDN), a family of membrane
spanning proteins that generate a barrier or a pore between two adjacent
epithelial cells. Many insights into molecular mechanisms of Mg(2+) handling have
been achieved by the identification of alterations and mutations in human genes
which cause disorders of paracellular Mg(2+) pathways (CLDN10, CLDN14, CLDN16,
CLDN19). Also, in the distal convoluted tubule, a basolateral protein, CNNM2,
causes if mutated, familial dominant and also recessive renal Mg(2+) wasting,
albeit its true function has not been clarified yet, but is assumed to play a key
role in the transcellular pathway. Moreover, mutations in human genes that are
involved in regulating these proteins directly or indirectly cause, if mutated
human diseases, mostly in combination with comorbidities as diabetes, cystic
renal disease, or metabolic abnormalities. Generation and characterization of
animal models harboring the corresponding mutations have further contributed to
the elucidation of physiology and pathophysiology of Mg(2+) disorders. Finally,
high-end crystallization techniques allow understanding of Mg(2+) handling in
more detail. As this field is rapidly growing, we describe here the principles of
physiology and pathophysiology of epithelial transport of renal Mg(2+)
homeostasis with emphasis on recently identified mechanisms involved.
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