Magnesium in Man: Implications for Health and Disease
Physiological Reviews Published 1 January 2015 Vol. 95 no. 1, 1-46 DOI: 10.1152/physrev.00012.2014
Jeroen H. F. de Baaij , Joost G. J. Hoenderop , René J. M. Bindels
Magnesium (Mg2+) is an essential ion to the human body, playing an instrumental role in supporting and sustaining health and life. As the second most abundant intracellular cation after potassium, it is involved in over 600 enzymatic reactions including energy metabolism and protein synthesis. Although Mg2+ availability has been proven to be disturbed during several clinical situations, serum Mg2+ values are not generally determined in patients. This review aims to provide an overview of the function of Mg2+ in human health and disease. In short, Mg2+ plays an important physiological role particularly in the brain, heart, and skeletal muscles. Moreover, Mg2+ supplementation has been shown to be beneficial in treatment of, among others,
- preeclampsia,
- migraine,
- depression,
- coronary artery disease, and
- asthma.
Over the last decade, several hereditary forms of hypomagnesemia have been deciphered, including mutations in transient receptor potential melastatin type 6 (TRPM6), claudin 16, and cyclin M2 (CNNM2).
Recently, mutations in Mg2+ transporter 1 (MagT1) were linked to T-cell deficiency underlining the important role of Mg2+ in cell viability.
Moreover, hypomagnesemia can be the consequence of the use of certain types of drugs, such as
- diuretics,
- epidermal growth factor receptor inhibitors,
- calcineurin inhibitors, and
- proton pump inhibitors.
This review provides an extensive and comprehensive overview of Mg2+ research over the last few decades, focusing on the regulation of Mg2+ homeostasis in the intestine, kidney, and bone and disturbances which may result in hypomagnesemia.
| I. | INTRODUCTION |
| II. | MAGNESIUM IN CELLULAR PHYSIOLOGY |
| III. | REGULATION OF MAGNESIUM HOMEOSTASIS |
| IV. | MAGNESIUM IN PHYSIOLOGY AND PATHOPHYSIOLOGY |
| V. | DISTURBANCES OF MAGNESIUM HOMEOSTASIS |
| VI. | CONCLUDING REMARKS |
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