Departments of Cell Biology and Ophthalmology, SUNY Downstate Medical center NY, Brooklyn, NY 11203, USA.
Adv Exp Med Biol. 2010;703:95-104. doi: 10.1007/978-1-4419-5635-4_7.
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.
慢性开角型青光眼是一种退行性视神经病变，可导致失明。我们已经表明，在疾病的动物模型以及人类中，改变表达的主要基因之一是补体成分 C1q。这些观察结果以及视网膜内其他补体成分上调的证据表明补体在该疾病的发病机制中起作用。我们回顾了支持这种作用的现有证据，并讨论了补体可能起作用的可能机制。深入了解这些机制对于我们合理设计新的治疗方法非常重要。
