Abstract

AbstractMüller cells support physiological neuronal activity and the integrity of the blood‐retinal barrier. A major function of Müller cells is the fluid absorption from the retinal tissue, which is mediated by transcellular water transport coupled to currents through potassium channels. In various disorders as retinal ischemia, ocular inflammation and /or retinal detachment, it was shown that Müller cells decrease the expression of the potassium channel (Kir4.1) which leads to an impairment of the water transport across Müller cell membranes, and induces the cellular swelling. Osmotic swelling of Müller cells is also induced by oxidative stress and by inflammatory mediators. The data suggest that a disturbed fluid transport through Müller cells is (in addition to vascular leakage) a pathogenic factor contributing to the development of retinal edema. Pharmacological re‐activation of the retinal water clearance by Müller cells may be used for treatment of macular edema. Intravitreal steroids as triamcinolone acetonide prevent osmotic swelling of Müller cells and induce the release of endogenous adenosine and subsequent A1 receptor activation which results in the opening of ion channels. Apparently, steroids resolve the edema by both inhibition of vascular leakage and stimulation of retinal fluid clearance by Müller cells.

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