摘要青光眼是我国及全球主要的致盲眼病.目前开角型青光眼的治疗局限于通过降低眼压延缓视神经病变的进展.临床用于降低眼压的药物主要机制为增强葡萄膜巩膜通路的房水外流和抑制房水生成.由于青光眼眼压升高的主要原因是小梁网通路阻力上升,因此现有药物未能从根本上纠正疾病的起源和病理生理改变.本文对直接针对青光眼小梁网房水外流阻塞病理机制的新药物靶点和治疗策略进行综述,以期这些新药物靶点和策略成为治疗青光眼的突破性新方法.

abstractsGlaucoma is a major cause of blindness in China and the world.Currently,all therapeutic means in treating open-angle glaucoma are limited to control the progression of optic neuropathy by lowering intraocular pressure (lOP).Clinically available medicines lower IOP by either enhancing the uveoscleral pathway or inhibiting aqueous humor production.Since the primary cause of IOP elevation in POAG is elevated outflow resistance in the trabecular outflow pathway,current medicines are not able to correct the underlying pathogenesis and pathophysiology of the disease.In this review article,we discuss a series of new therapeutic targets and therapeutic approaches that are designed to directly modify the pathological changes related to the reduction in trabecular outflow in glaucoma patients.Some of these targets and approaches may produce a significant breakthrough in the treatment of this devastating disease.