Sorbonne Université, INSERM, CNRS, Institut de la Vision, 17 rue Moreau, F-75012 Paris, France.
Service de NeuroImagerie, Centre Hospitalier National d'ophtalmologie des Quinze-Vingts, F-75012 Paris, France.
Cells. 2020 Feb 25;9(3):535. doi: 10.3390/cells9030535.
Glaucoma is one of the leading causes of irreversible blindness in the world and remains a major public health problem. To date, incomplete knowledge of this disease's pathophysiology has resulted in current therapies (pharmaceutical or surgical) unfortunately having only a slowing effect on disease progression. Recent research suggests that glaucomatous optic neuropathy is a disease that shares common neuroinflammatory mechanisms with "classical" neurodegenerative pathologies. In addition to the death of retinal ganglion cells (RGCs), neuroinflammation appears to be a key element in the progression and spread of this disease. Indeed, early reactivity of glial cells has been observed in the retina, but also in the central visual pathways of glaucoma patients and in preclinical models of ocular hypertension. Moreover, neuronal lesions are not limited to retinal structure, but also occur in central visual pathways. This review summarizes and puts into perspective the experimental and clinical data obtained to date to highlight the need to develop neuroprotective and immunomodulatory therapies to prevent blindness in glaucoma patients.
青光眼是世界上导致不可逆性失明的主要原因之一，仍然是一个主要的公共卫生问题。迄今为止，由于对这种疾病的病理生理学认识不完整，目前的治疗方法（药物或手术）不幸仅对疾病进展有减缓作用。最近的研究表明，青光眼视神经病变是一种与“经典”神经退行性病变具有共同神经炎症机制的疾病。除了视网膜神经节细胞（RGC）的死亡外，神经炎症似乎是该疾病进展和传播的关键因素。事实上，已经在青光眼患者的视网膜以及中央视觉通路中观察到了胶质细胞的早期反应，并且在眼压升高的临床前模型中也是如此。此外，神经元损伤不仅限于视网膜结构，还发生在中央视觉通路上。这篇综述总结并分析了迄今为止获得的实验和临床数据，以强调需要开发神经保护和免疫调节疗法来预防青光眼患者的失明。
