Tthe role of low-grade inflammation in glaucoma

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Glaucoma has been associated with low-grade inflammation. The exact role of inflammatory processes in the pathophysiology of various types of glaucoma is, however, unclear. In addition, few in vivo studies have provided direct evidence for inflammatory processes in glaucoma. Disturbed auto regulation has been shown to increase the levels of Endothelin-1 (ET-1) and/or nitric oxide (NO) thereby causing inflammation by either inducing ischemia or oxidative stress. Evidence has furthermore revealed a diminished Müller cell ability to remove excess glutamate in the synaptic cleft in response to vascular dysregulation. This in turn causes glutamate excitotoxicity with a hyperstimulation of the NMDA receptor. Activation of NMDA-receptors has been shown to induce TNF-α production in the Müller cells, indirectly causing RGC death through TNF-α stimulation of TNF-α receptor 1 on RGC. Specifically, this aspect of RGC death rise the possible involvement of low-grade inflammation as an important factor in the metabolic and excitotoxic intradependance between Müller cells and RGC. The current knowledge of low-grade inflammatory changes in glaucoma and ideas on possible future targets for pharmaceutical intervention in glaucoma will be discussed

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