Rho激酶抑制剂对青光眼的神经保护作用及研究进展

Effects of Rho associated kinase inhibitors on glaucoma and current researches

青光眼是全球主要的致盲眼病之一，以最终导致视网膜神经节细胞（RGCs）逐渐凋亡及其轴突丢失为主要特征。目前，降低眼压是控制青光眼发展的主要治疗方式，然而，并不是所有的患者都适用于该疗法，这与青光眼的病理生理过程并不只是由眼压升高引起有关。针对青光眼发病的多因素，迫切需要寻找新的治疗策略。新疗法的重点应放在预防或延缓RGCs的凋亡、修复损伤的轴突上，因此青光眼视神经保护治疗已成为目前研究的热点。Rho激酶（ROCK）抑制剂作为可以降低眼压、抑制抗青光眼术后瘢痕形成、改善眼部血液循环、提高RGCs存活率、防止轴突变性以及诱导轴突再生的实验阶段药物，已成为目前新药研究的热点。本文将重点对ROCK抑制剂的经典信号通路在青光眼视神经保护方面的研究现状及进展进行综述。

Glaucoma is one of the main causes of blindness in the world, resulting from a slow and progressive loss of retinal ganglion cells （RGCs） and their axons. So far, intraocular pressure reduction is the main treatment modality to control disease progression. However, not all the patients benefit from this therapy, and the pathophysiology of glaucoma is not always associated with an elevated intraocular pressure. These limitations, together with the muhifactorial etiology of glaucoma, urge the pressing medical need for novel and alternative treatment strategies. Such new therapies should focus on not only preventing or retarding RGCs death, but also repairing the injured axons. Glaucoma optic nerve protection therapy is becoming a hot spot of current research, especially Rho associated kinase （ROCK） inhibitors as a new drug for the glaucomatic neuroprotection,which can reduce intraocular pressure,inhibit scar formation after anti-glaucoma surgery,improve blood circulation,prevent RGCs death and axonal degeneration and induce axon regeneration. In this review, we focused on the research status and progress of the classical signal pathway of ROCK inhibitor in glaucoma optic nerve protection.