Abstract:This review article is focused on the various facets of possible endothelin's role in glaucoma; involvement of endothelin in other ocular, in particular vascular, diseases is not specifically discussed. Endothelin is an ubiquitous molecule that occurs in practically all ocular tissues. Its primary physiological function is regulation of the blood vessel diameter and hence regulation of the blood supply in tissues. It is secreted locally, and exerts its effect also predominantly locally. This limits the value o… Show more
“…Gugleta, et al, [24] described the significance of endothelin-1 in glaucoma. Endothelin-1 is vasoconstrictive and is a ubiquitous molecule that occurs in nearly all tissues.…”
Section: American Journal Of Biomedical Science and Researchmentioning
Normal tension glaucoma is the most common form of glaucoma among people of Asian countries. While treatment to lower pressure in normal tension glaucoma is the standard of care, this is universally acknowledged as insufficient to the task. Recent evidence implicates ischemia and oxidative stress as key stressors of the optic nerve in normal tension glaucoma. Addressing ischemia and oxidative stress have been recommended as neuroprotective strategies. Elevated retinal venous pressure is found in normal tension glaucoma, and this venous hypertension is not adequately addressed with current medications. It increases resistance and reduces perfusion resulting in oxidative stress and localized ischemia. Elevated RVP appears to also be a factor in small vessel ischemia in diabetic retinopathy and macular degeneration.The cause of elevated retinal venous pressure is small vessel endotheliopathy. Endotheliopathic damage may be caused by derangement of methylation and B-vitamin metabolism, resulting in altered microcirculation. This metabolic derangement may be due to either dietary inadequacies, malabsorption, or genetic polymorphisms of the methylation pathways. Restoration of folate and B-12 plasma levels may be accomplished with supplementation using natural forms of these vitamins, specifically L-methylfolate and methylcobalamin. Use of oxidized folate (folic acid) penetrates the blood retinal barrier only after enzymatic converstion of the folic acid to methylfolate. Since there is a limited capacity for folic acid conversion, excess folic acid remains unmetabolized and impedes methylfolate absorption into the retina. Thus, successful nutritional supplementation must employ methylfolate and not folic acid. Such nutritional approaches are valuable adjuncts to standard ophthalmologic treatment, lowering retinal venous pressure and improving perfusion. Improved supply of micronutrients has implications for management of ischemic optic neuropathies, including normal tension glaucoma, nonarteritic ischemic optic neuropathy, and diabetic optic neuropathy and retinopathy.
“…Gugleta, et al, [24] described the significance of endothelin-1 in glaucoma. Endothelin-1 is vasoconstrictive and is a ubiquitous molecule that occurs in nearly all tissues.…”
Section: American Journal Of Biomedical Science and Researchmentioning
Normal tension glaucoma is the most common form of glaucoma among people of Asian countries. While treatment to lower pressure in normal tension glaucoma is the standard of care, this is universally acknowledged as insufficient to the task. Recent evidence implicates ischemia and oxidative stress as key stressors of the optic nerve in normal tension glaucoma. Addressing ischemia and oxidative stress have been recommended as neuroprotective strategies. Elevated retinal venous pressure is found in normal tension glaucoma, and this venous hypertension is not adequately addressed with current medications. It increases resistance and reduces perfusion resulting in oxidative stress and localized ischemia. Elevated RVP appears to also be a factor in small vessel ischemia in diabetic retinopathy and macular degeneration.The cause of elevated retinal venous pressure is small vessel endotheliopathy. Endotheliopathic damage may be caused by derangement of methylation and B-vitamin metabolism, resulting in altered microcirculation. This metabolic derangement may be due to either dietary inadequacies, malabsorption, or genetic polymorphisms of the methylation pathways. Restoration of folate and B-12 plasma levels may be accomplished with supplementation using natural forms of these vitamins, specifically L-methylfolate and methylcobalamin. Use of oxidized folate (folic acid) penetrates the blood retinal barrier only after enzymatic converstion of the folic acid to methylfolate. Since there is a limited capacity for folic acid conversion, excess folic acid remains unmetabolized and impedes methylfolate absorption into the retina. Thus, successful nutritional supplementation must employ methylfolate and not folic acid. Such nutritional approaches are valuable adjuncts to standard ophthalmologic treatment, lowering retinal venous pressure and improving perfusion. Improved supply of micronutrients has implications for management of ischemic optic neuropathies, including normal tension glaucoma, nonarteritic ischemic optic neuropathy, and diabetic optic neuropathy and retinopathy.
ZusammenfassungDas gleichzeitige Auftreten von Schlafstörungen und Glaukom könnte in einem Zusammenhang stehen. Es gibt bisher keine konkreten Studien darüber, wie häufig und warum Schlafstörungen bei Glaukompatienten auftreten, jedoch liegen verschiedene Ansätze vor, die sowohl einen Zusammenhang zwischen dem Auftreten von Schlafstörungen im Verlauf einer Glaukomerkrankung als auch zwischen dem Auftreten eines Glaukoms und bestimmten Schlafgewohnheiten herstellen.
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