摘要
青光眼是一組以視網膜神經節細胞進行性變性為特徵的視神經病變，患者主要會出現視神經萎縮、視野缺損和視功能逐漸喪失的特徵，是全球第二大失明的主要原因。預測到2040年，全球青光眼的人數將增加到1.118億。 因為大部分青光眼是由病理性高眼壓引起，所以降低眼內壓是預防及治療青光眼的主要途徑。 本文章綜述了三種新型療法，Rho激酶抑製劑、一氧化氮-可溶性鳥苷酸環化酶通路以及腎素-血管緊張素系統中在降低眼內壓的生理機制以及在治療青光眼的研究結論。Rho激酶抑制劑信號通路不單參與了青光眼的發病機制，還在降低眼內壓、保護視網膜神經節細胞及改善眼部血流量方面扮演著一定的角色，因此特異性Rho激酶抑制劑可能成為青光眼治療的一個新的靶點。另外，低濃度的一氧化氮與青光眼的發病具有密切關係，會藉由調節眼內壓、眼血流及影響細胞凋亡等作用機制影響青光眼的病理發展。而在腎素-血管緊張素系統中則是以減少睫狀體的血流量來減少房水的產生，因此可在青光眼中發揮神經保護作用，並且它們還可能具有治療和預防糖尿病性視網膜病的潛力。
並列摘要
Glaucoma represents a group of optic neuropathies characterized by progressive degeneration of retinal ganglion cells. The main manifestations include optic neural atrophy, visual field defect, and gradual loss of visual functions. Glaucoma is the second leading cause of global blindness. By the year 2040, it is estimated that glaucomatous patients will increase to be about 111.8 million. Since glaucoma is mostly caused by pathological increase of intraocular pressure (IOP), reduction of IOP is the main route for prevention and treatment. This assay will discuss three novel therapeutic pathways, Rho kinase inhibitor, nitric oxide-soluble guanylate cyclase, and renin-angiotensin system, regarding their underlying emchanisms and current research findingds. Rho kinase inhibitor prevents the pathogenesis of glaucoma, reduces IOP, protects retinal glanglion cells, and regulates ocualr blood flow volume. Thus, specific Rho kinase inhibitor may potentially be a novel therapeutic target. Besides, low concentrations of nitric oxide have been found to be closely related to the pathogenesis of glaucoma, through regulation of IOP, blood flow volume, and apoptosis of retinal ganglion cells. Compounds acting on the RAS may also exert a neuroprotective effect in glaucoma, and they may also have a potential for treatment and prevention of diabetic retinopathy, a leading cause of blindness in people of working age.