TLR4在青光眼视神经损伤机制中的作用

青光眼是一种以视乳头萎缩凹陷、视野缺损及视力下降为共同特征的不可逆的致盲性疾病,其视神经损伤的本质为视神经节细胞的凋亡。尽管通过药物干预和手术控制眼压可以对青光眼起到一定的治疗作用,但如何从根本上阻止青光眼的进一步发展仍处于探索阶段。因此,研究青光眼视神经损伤机制,通过阻断视神经损伤而治疗青光眼至关重要。近几年,免疫机制对青光眼视神经损伤的影响成为研究热点,本文中主要对Toll样受体4(TLR4)通过不同免疫通路并与神经胶质细胞相互作用引起青光眼患者视神经损伤进行综述。

The role of TLR4 in the mechanism of optic nerve injury in glaucoma

Glaucoma is a kind of irreversible blind disease characterized by atrophyand depression of optic papilla, visual field defect and vision decline. The essence of optic nerve injury is the death of optic ganglion cells. Although controlling intraocular pressure through drugs and surgery can play a certain role in the treatment of glaucoma, how to fundamentally prevent the further development of glaucoma is still in the exploratory stage. Therefore, studying the mechanism of optic nerve injury in glaucoma is very important to treat glaucoma. In recent years, the immune mechanism on optic nerve injury in glaucoma has become a hot. In this paper, how TLR4 induces optic nerve injury in glaucoma patients was reviewed, with different immune pathways and interaction with the neuroglial.