Magnesium Regulates Endothelial Barrier Functions through TRPM7, MagT1, and S1P1
Abstract
Abstract Mg 2+ ‐deficiency is linked to hypertension, Alzheimer's disease, stroke, migraine headaches, cardiovascular diseases, and diabetes, etc., but its exact role in these pathophysiological conditions remains elusive. Mg 2+ can regulate vascular functions, yet the mechanistic insight remains ill‐defined. Data show that extracellular Mg 2+ enters endothelium mainly through the TRPM7 channel and MagT1 transporter. Mg 2+ can act as an antagonist to reduce Ca 2+ signaling in endothelium. Mg 2+ also reduces the intracellular reactive oxygen species (ROS) level and inflammation. In addition, Mg 2+ ‐signaling increases endothelial survival and growth, adhesion, and migration. Endothelial barrier integrity is significantly enhanced with Mg 2+ ‐treatment through S1P1‐Rac1 pathways and barrier‐stabilizing mediators including cAMP, FGF1/2, and eNOS. Mg 2+ also promotes cytoskeletal reorganization and junction proteins to tighten up the barrier. Moreover, Mg 2+ ‐deficiency enhances endothelial barrier permeability in mice, and Mg 2+ ‐treatment rescues histamine‐induced transient vessel hyper‐permeability in vivo. In summary, Mg 2+ ‐deficiency can cause deleterious effects in endothelium integrity, and Mg 2+ ‐treatment may be effective in the prevention or treatment of vascular dysfunction.
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