The pathophysiology of glaucoma is complex, multifactorial and not completely understood. Elevated intraocular pressure (IOP) and/or impaired retinal blood flow may cause initial optic nerve damage. In addition, age-related oxidative stress in the retina concurrently with chronic mechanical and vascular stress is crucial for the initiation of retinal neurodegeneration. Oxidative stress is closely related to cell senescence, mitochondrial dysfunction, excitotoxicity, and neuroinflammation, which are involved in glaucoma progression. Accumulating evidence from animal glaucoma models and from human ocular samples suggests a dysfunction of the para-inflammation in the retinal ganglion cell layer and the optic nerve head. Moreover, quite similar mechanisms in the anterior chamber could explain the trabecular meshwork dysfunction and the elevated IOP in primary open-angle glaucoma. On the other hand, ocular surface disease due to topical interventions is the most prominent and visible consequence of inflammation in glaucoma, with a negative impact on filtering surgery failure, topical treatment efficacy, and possibly on inflammation in the anterior segment. Consequently, glaucoma appears as an outstanding eye disease where inflammatory changes may be present to various extents and consequences along the eye structure, from the ocular surface to the posterior segment, and the visual pathway. Here we reviewed the inflammatory processes in all ocular structures in glaucoma from the back to the front of the eye and beyond. Our approach was to explain how para-inflammation is necessary to maintain homoeostasis, and to describe abnormal inflammatory findings observed in glaucomatous patients or in animal glaucoma models, supporting the hypothesis of a dysregulation of the inflammatory balance toward a pro-inflammatory phenotype. Possible anti-inflammatory therapeutic approaches in glaucoma are also discussed.

青光眼的病理生理学是复杂的、多因素的且尚未完全了解。升高的眼内压 (IOP) 和/或受损的视网膜血流可能会导致最初的视神经损伤。此外，视网膜中与年龄相关的氧化应激以及慢性机械和血管应激对于视网膜神经变性的启动至关重要。氧化应激与细胞衰老、线粒体功能障碍、兴奋性毒性和神经炎症密切相关，这些都参与了青光眼的进展。来自动物青光眼模型和人类眼部样本的累积证据表明，视网膜神经节细胞层和视神经乳头的副炎症功能障碍。而且，前房中非常相似的机制可以解释小梁网功能障碍和原发性开角型青光眼的眼压升高。另一方面，由于局部干预引起的眼表疾病是青光眼炎症最突出和最明显的后果，对滤过手术失败、局部治疗效果以及可能对眼前节炎症产生负面影响。因此，青光眼似乎是一种突出的眼病，其中炎症变化可能会在眼睛结构中出现不同程度和后果，从眼表到后段，以及视觉通路。在这里，我们回顾了青光眼从眼睛后部到前部及其他部位的所有眼部结构的炎症过程。我们的方法是解释副炎症如何是维持稳态所必需的，并描述在青光眼患者或动物青光眼模型中观察到的异常炎症结果，支持炎症平衡失调向促炎表型的假设。还讨论了青光眼可能的抗炎治疗方法。