Magnesium homeostasis and therapy in hypertension

Author(s):  
Klaus Kisters ◽  
Hans-Georg Classen ◽  
Jürgen Vormann ◽  
Tanja Werner ◽  
Ronald Smetana ◽  
...  

2018 ◽  
Vol 20 (2) ◽  
pp. 150-169
Author(s):  
Ja.F. Zverev ◽  
◽  
V.M. Bryukhanov ◽  
A.Ya. Rykunova ◽  
◽  
...  


Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2169
Author(s):  
Dominique Bayle ◽  
Cécile Coudy-Gandilhon ◽  
Marine Gueugneau ◽  
Sara Castiglioni ◽  
Monica Zocchi ◽  
...  

Chronic Mg2+ deficiency is the underlying cause of a broad range of health dysfunctions. As 25% of body Mg2+ is located in the skeletal muscle, Mg2+ transport and homeostasis systems (MgTHs) in the muscle are critical for whole-body Mg2+ homeostasis. In the present study, we assessed whether Mg2+ deficiency alters muscle fiber characteristics and major pathways regulating muscle physiology. C57BL/6J mice received either a control, mildly, or severely Mg2+-deficient diet (0.1%; 0.01%; and 0.003% Mg2+ wt/wt, respectively) for 14 days. Mg2+ deficiency slightly decreased body weight gain and muscle Mg2+ concentrations but was not associated with detectable variations in gastrocnemius muscle weight, fiber morphometry, and capillarization. Nonetheless, muscles exhibited decreased expression of several MgTHs (MagT1, CNNM2, CNNM4, and TRPM6). Moreover, TaqMan low-density array (TLDA) analyses further revealed that, before the emergence of major muscle dysfunctions, even a mild Mg2+ deficiency was sufficient to alter the expression of genes critical for muscle physiology, including energy metabolism, muscle regeneration, proteostasis, mitochondrial dynamics, and excitation–contraction coupling.



2003 ◽  
Vol 27 (9) ◽  
pp. 853-857 ◽  
Author(s):  
Kostas P. Katopodis ◽  
Elli L. Koliousi ◽  
Emilios K. Andrikos ◽  
Michael V. Pappas ◽  
Moses S. Elisaf ◽  
...  


1982 ◽  
Vol 72 (3) ◽  
pp. 473-488 ◽  
Author(s):  
Zalman S. Agus ◽  
Alan Wasserstein ◽  
Stanley Goldfarb


Author(s):  
Vladimir Chubanov ◽  
Jonathan T. Eggenschwiler ◽  
Lillia V. Ryazanova ◽  
Thomas Gudermann ◽  
Alexey G. Ryazanov


2010 ◽  
pp. 110-124
Author(s):  
George Samandouras

Chapter 3.2 discusses fluid and electrolyte problems in neurosurgery, including fluid homeostasis disorders, sodium homeostasis disorders, potassium homeostasis disorders, calcium homeostasis disorders, magnesium homeostasis disorders, and acid-base disorders.



2019 ◽  
Vol 116 (8) ◽  
pp. 2925-2934 ◽  
Author(s):  
Serge Hardy ◽  
Elie Kostantin ◽  
Shan Jin Wang ◽  
Tzvetena Hristova ◽  
Gabriela Galicia-Vázquez ◽  
...  

Phosphatases of regenerating liver (PRL-1, PRL-2, and PRL-3, also known as PTP4A1, PTP4A2, and PTP4A3) control magnesium homeostasis through an association with the CNNM magnesium transport regulators. Although high PRL levels have been linked to cancer progression, regulation of their expression is poorly understood. Here we show that modulating intracellular magnesium levels correlates with a rapid change of PRL expression by a mechanism involving its 5′UTR mRNA region. Mutations or CRISPR-Cas9 targeting of the conserved upstream ORF present in the mRNA leader derepress PRL protein synthesis and attenuate the translational response to magnesium levels. Mechanistically, magnesium depletion reduces intracellular ATP but up-regulates PRL protein expression via activation of the AMPK/mTORC2 pathway, which controls cellular energy status. Hence, altered PRL-2 expression leads to metabolic reprogramming of the cells. These findings uncover a magnesium-sensitive mechanism controlling PRL expression, which plays a role in cellular bioenergetics.



PLoS Genetics ◽  
2019 ◽  
Vol 15 (8) ◽  
pp. e1008336 ◽  
Author(s):  
Emilie Trachsel ◽  
Peter Redder ◽  
Patrick Linder ◽  
Joshua Armitano


2018 ◽  
Vol 475 (6) ◽  
pp. 1129-1139 ◽  
Author(s):  
Atsushi Yoshida ◽  
Yosuke Funato ◽  
Hiroaki Miki

Phosphatase of regenerating liver (PRL) is highly expressed in malignant cancers and promotes cancer progression. Recent studies have suggested its functional relationship with Mg2+, but the importance and molecular details of this relationship remain unknown. Here, we report that PRL expression is regulated by Mg2+ and PRL protects cells from apoptosis under Mg2+-depleted conditions. When cultured cells were subjected to Mg2+ depletion, endogenous PRL protein levels increased significantly. siRNA-mediated knockdown of endogenous PRL did not significantly affect cell proliferation under normal culture conditions, but it increased cell death after Mg2+ depletion. Imaging analyses with a fluorescent probe for Mg2+ showed that PRL knockdown severely reduced intracellular Mg2+ levels, indicating a role for PRL in maintaining intracellular Mg2+. We also examined the mechanism of augmented expression of PRL proteins and found that PRL mRNA transcription was stimulated by Mg2+ depletion. A series of analyses revealed the activation and the crucial importance of signal transducer and activator of transcription 1 in this process. Collectively, these results implicate PRL in maintaining cellular Mg2+ homeostasis.



2019 ◽  
Vol 34 (4) ◽  
pp. 380-390 ◽  
Author(s):  
Young M. Jeong ◽  
Cristiano Dias ◽  
Casey Diekman ◽  
Helene Brochon ◽  
Pyonghwa Kim ◽  
...  

The circadian clock controls 24-h biological rhythms in our body, influencing many time-related activities such as sleep and wake. The simplest circadian clock is found in cyanobacteria, with the proteins KaiA, KaiB, and KaiC generating a self-sustained circadian oscillation of KaiC phosphorylation and dephosphorylation. KaiA activates KaiC phosphorylation by binding the A-loop of KaiC, while KaiB attenuates the phosphorylation by sequestering KaiA from the A-loop. Structural analysis revealed that magnesium regulates the phosphorylation and dephosphorylation of KaiC by dissociating from and associating with catalytic Glu residues that activate phosphorylation and dephosphorylation, respectively. High magnesium causes KaiC to dephosphorylate, whereas low magnesium causes KaiC to phosphorylate. KaiC alone behaves as an hourglass timekeeper when the magnesium concentration is alternated between low and high levels in vitro. We suggest that a magnesium-based hourglass timekeeping system may have been used by ancient cyanobacteria before magnesium homeostasis was established.



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