Glaucoma is a degenerative process of the optic nerve. Increased intraocular pressure is believed to be the main factor leading to the glaucomatous damage. The in vitro and in vivo animal glaucoma research models provide insight into the molecular changes in the retina in response to the injury factor. The damage is a complex process incorporating molecular and immunological changes. Such changes involve NFκB activity and complement activation. The processes affect the human antigen, JNK, MAPK, p53, MT2 and DBA/2J molecular pathways, activate the autophagy processes and compromise neuroprotective mechanisms. Activation and inhibition of immunological responses contribute to cell injury. The immunological mechanisms of glaucomatous degeneration include glial response, the complement, tumor necrosis factor α (TNF-α) pathways and toll-like receptors athways. Oxidative stress and excitotoxicity are factors contributing to cell death in glaucoma. The authors present an up-to-date review of the mechanisms involved and update on research focusing on a possible innovative glaucoma treatment.

中文翻译：

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原发性开角型青光眼病理机制的免疫学和分子基础

青光眼是视神经的退行性过程。眼内压升高被认为是导致青光眼损害的主要因素。体外和体内动物青光眼研究模型提供了对视网膜响应损伤因素的分子变化的深入了解。损伤是一个包含分子和免疫学变化的复杂过程。这些变化涉及 NFκB 活性和补体激活。这些过程影响人类抗原、JNK、MAPK、p53、MT2 和 DBA/2J 分子通路，激活自噬过程并损害神经保护机制。免疫反应的激活和抑制会导致细胞损伤。青光眼变性的免疫学机制包括神经胶质反应、补体、肿瘤坏死因子α（TNF-α）途径和Toll样受体途径。氧化应激和兴奋性毒性是导致青光眼细胞死亡的因素。作者对所涉及的机制进行了最新回顾，并更新了关注可能的创新青光眼治疗方法的研究进展。