Magnesium is the physiologic calcium channel blocker, involving in many different metabolic processes by maintaining cell membrane function, modulating smooth muscle contraction and influencing enzymatic activities. Magnesium has been shown to increase blood flow to tissues by modifying endothelial function via endothelin-1 (ET-1) and nitric Oxide (NO) pathways. Magnesium also exhibits neuroprotective role by blocking N-methyl-D-aspartate (NMDA) receptor related calcium influx and by inhibiting the release of glutamate, hence protects the cell against oxidative stress and apoptosis. Both increase in blood flow and its neuroprotective effect make magnesium a good candidate for glaucoma studies. Magnesium has been shown to decrease oxidative stress and apoptosis in retinal tissue and to have retinal ganglion cell sparing effect. A series of studies has been conducted about magnesium could decrease insulin resistance in diabetic patients, ease glycemia control and prevent diabetic retinopathy. Magnesium is found to be critically important in maintaining normal ionic homeostasis of lens. Magnesium deficiency has been shown to cause increased lenticular oxidative stress and ionic imbalance in the lens so trigger cataractogenesis.
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.