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      The Role of Magnesium in the Pathogenesis and Treatment of Glaucoma

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          Abstract

          Glaucoma is characterized by chronic optic neuropathy resulting in progressive vision loss. Not only is glaucoma considered as a condition of elevated intraocular pressure (IOP), but also other risk factors may play a role in the pathogenesis of glaucomatous optic nerve damage. Vascular dysregulation in ocular blood flow and oxidative stress are currently suggested as important risk factors for glaucomatous retinal ganglion cell loss. New treatment modalities that improve ocular blood flow and reduce oxidative stress have been investigated in many studies. Magnesium (Mg) is thought to be one of the molecules that has a treatment potential in glaucoma. Mg has been shown to improve blood flow by modifying endothelial function via endothelin-1 (ET-1) and endothelial nitric oxide (NO) pathways. Mg also exhibits neuroprotective role by blocking N-methyl-D-aspartate (NMDA) receptor-related calcium influx and by inhibiting the release of glutamate, and hence protects the cell against oxidative stress and apoptosis. Both improvement in ocular blood flow and prevention of ganglion cell loss would make magnesium a good candidate for glaucoma management. Further studies on the effect of Mg may open a new therapeutic era in glaucoma.

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          Most cited references81

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          Oxidative stress and mitochondrial dysfunction in glaucoma.

          Mitochondrial dysfunction increases reactive oxygen species (ROS) production and when this overwhelms the cellular antioxidant defences, oxidative stress ensues. Oxidative stress is recognized as a common pathologic pathway in many neurodegenerative diseases. Recent reports have also demonstrated oxidative stress in ocular tissues derived from experimental glaucoma models and clinical samples. There is also accumulating evidence pointing to mitochondrial dysfunction being present in some glaucoma patients. Thus oxidative stress from mitochondrial dysfunction may also play a causal role in glaucoma. The mechanisms by which oxidative stress may induce retinal ganglion cell loss in glaucoma are not fully understood but could include direct neurotoxic effects from ROS or indirect damage from oxidative stress-induced dysfunction of glial cells. This review will consider the evidence for the presence of oxidative stress in glaucoma; the mechanisms by which oxidative stress may contribute to disease pathogenesis; and also consider therapeutic approaches that target oxidative stress as a means of protecting against optic nerve degeneration. Copyright © 2012 Elsevier Ltd. All rights reserved.
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            The primary vascular dysregulation syndrome: implications for eye diseases

            Vascular dysregulation refers to the regulation of blood flow that is not adapted to the needs of the respective tissue. We distinguish primary vascular dysregulation (PVD, formerly called vasospastic syndrome) and secondary vascular dysregulation (SVD). Subjects with PVD tend to have cold extremities, low blood pressure, reduced feeling of thirst, altered drug sensitivity, increased pain sensitivity, prolonged sleep onset time, altered gene expression in the lymphocytes, signs of oxidative stress, slightly increased endothelin-1 plasma level, low body mass index and often diffuse and fluctuating visual field defects. Coldness, emotional or mechanical stress and starving can provoke symptoms. Virtually all organs, particularly the eye, can be involved. In subjects with PVD, retinal vessels are stiffer and more irregular, and both neurovascular coupling and autoregulation capacity are reduced while retinal venous pressure is often increased. Subjects with PVD have increased risk for normal-tension glaucoma, optic nerve compartment syndrome, central serous choroidopathy, Susac syndrome, retinal artery and vein occlusions and anterior ischaemic neuropathy without atherosclerosis. Further characteristics are their weaker blood–brain and blood-retinal barriers and the higher prevalence of optic disc haemorrhages and activated astrocytes. Subjects with PVD tend to suffer more often from tinnitus, muscle cramps, migraine with aura and silent myocardial ischaemic and are at greater risk for altitude sickness. While the main cause of vascular dysregulation is vascular endotheliopathy, dysfunction of the autonomic nervous system is also involved. In contrast, SVD occurs in the context of other diseases such as multiple sclerosis, retrobulbar neuritis, rheumatoid arthritis, fibromyalgia and giant cell arteritis. Taking into consideration the high prevalence of PVD in the population and potentially linked pathologies, in the current article, the authors provide recommendations on how to effectively promote the field in order to create innovative diagnostic tools to predict the pathology and develop more efficient treatment approaches tailored to the person.
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              Magnesium: nature's physiologic calcium blocker.

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                Author and article information

                Journal
                Int Sch Res Notices
                Int Sch Res Notices
                ISRN
                International Scholarly Research Notices
                Hindawi Publishing Corporation
                2356-7872
                2014
                13 October 2014
                : 2014
                : 745439
                Affiliations
                1Department of Ophthalmology, Recep Tayyip Erdoğan University Medical School, 53020 Rize, Turkey
                2Department of Ophthalmology, Duzce State Hospital, 81100 Duzce, Turkey
                3Department of Ophthalmology, Sorgun State Hospital, 66700 Yozgat, Turkey
                4Department of Ophthalmology, Yatağan State Hospital, 48500 Muğla, Turkey
                5Department of Ophthalmology, Onsekizmart University Medical School, 17020 Canakkale, Turkey
                6Department of Ophthalmology, Gazi University Medical School, 06560 Ankara, Turkey
                7Department of Medical Pharmacology, Gazi University Medical School, 06560 Ankara, Turkey
                Author notes

                Academic Editor: Paolo Fogagnolo

                Author information
                http://orcid.org/0000-0002-3050-0714
                http://orcid.org/0000-0001-7124-4174
                Article
                10.1155/2014/745439
                4897098
                27433524
                06283747-ef8e-4831-a82a-8355aaf73719
                Copyright © 2014 Feyzahan Ekici et al.

                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.

                History
                : 19 April 2014
                : 25 June 2014
                : 16 July 2014
                Categories
                Review Article

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