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When EGF is offside, magnesium is wasted
Shmuel Muallem, Orson W. Moe
Shmuel Muallem, Orson W. Moe
Published August 1, 2007
Citation Information: J Clin Invest. 2007;117(8):2086-2089. https://doi.org/10.1172/JCI33004.
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Commentary

When EGF is offside, magnesium is wasted

Abstract

Our understanding of magnesium (Mg2+) regulation has recently been catapulted forward by the discovery of several disease loci for monogenic disorders of Mg2+ homeostasis. In this issue of the JCI, Groenestege et al. report that their study of a rare inherited Mg2+ wasting disorder in consanguineous kindred shows that EGF acts as an autocrine/paracrine magnesiotropic hormone (see the related article beginning on page 2260). EGF stimulates Mg2+ reabsorption in the renal distal convoluted tubule (DCT) via engagement of its receptor on the basolateral membrane of DCT cells and activation of the Mg2+ channel TRPM6 (transient receptor potential cation channel, subfamily M, member 6) in the apical membrane. These authors show that a point mutation in pro-EGF retains EGF secretion to the apical but not the basolateral membrane, disrupting this cascade and causing renal Mg2+ wasting. This work is another seminal example of the power of the study of monogenic disorders in the quest to understand human physiology.

Authors

Shmuel Muallem, Orson W. Moe

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