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Abstract
Abstract
Retinal Edema Development - a Failure of Glial Cells
Bringmann A., Pannicke T., Iandiev I., Uckermann O., Biedermann B., Reichenbach A., Wiedemann P.
Klinik und Poliklinik für Augenheilkunde, Universität Leipzig; Paul-Flechsig-Institut für Hirnforschung, Universität Leipzig
Macular edema, which contributes to photoreceptor degeneration and neuronal cell death, is an important complication in various diseases of the retina such as diabetic retinopathy and age-related macular degeneration. The relative importance of increased extracellular fluid versus swelling of Müller glial cells, which both can contribute to the development of macular edema, is uncertain. Swelling of Müller cells in the macula was described to frequently precede other signs of edema formation; and there are suggestions that the cysts in the cystoid macular edema are swollen Müller cells. However, while retinal ischemia was suggested to be one major factor which favor edema development, the pathogenesis of Müller cell swelling is unclear.
The high metabolic activity in the retina is accompanied by a strong influx of metabolic substrates such as glucose and lactate from the blood into the retinal tissue which is coupled to water influx. Additionally, oxidative ATP production is accompanied by the formation of a huge amount of water. There is a continuous water efflux from the retinal tissue into the blood and the vitreous, via Müller cell bodies. Müller cells express water channels, the aquaporins, in their plasma membranes for facilitation of the water fluxes. However, the water fluxes are coup