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Chronic open angle glaucoma is a degenerative optic neuropathy that can lead to blindness. We have shown that one of the major genes with altered expression in the glaucomatous retina is complement component C1q in both animal models of the disease as well as in humans. These observations together with evidence of upregulation of other complement components within the retina suggest a role for complement in the pathogenesis of this disease. We review the current evidence that supports such a role and discuss possible mechanisms through which complement may act. A thorough understanding of these mechanisms is important in allowing us to rationally design new therapeutic approaches.
L. Ren. Departments of Cell Biology and Ophthalmology, SUNY Downstate Medical center NY, Brooklyn, NY 11203, USA.
3.4.2 Gene studies (Part of: 3 Laboratory methods > 3.4 Molecular genetics)
3.9 Pathophysiology (Part of: 3 Laboratory methods)
3.10 Immunobiology (Part of: 3 Laboratory methods)
3.5 Molecular biology incl. SiRNA (Part of: 3 Laboratory methods)