Glaucoma is a leading cause of blindness worldwide. It is characterized by optic neuropathy and progressive concentric vision loss. Based on the status of the anterior chamber angle, glaucoma can be divided into open and closed angle glaucoma. Open angle glaucoma, especially primary open angle glaucoma, affects the majority of patients. Although primary open angle glaucoma and other open angle glaucomas have been studied for decades, the exact disease mechanisms are not clear. Numerous clinical studies have shown that elevated intraocular pressure is the primary risk factor and causative factor for the development and progression of open angle glaucoma.1
Lowering intraocular pressure has been found to be an effective method for preventing optic nerve damage and preserving vision.1
The current strategies for lowering intraocular pressure include decreasing aqueous humor production (β-blockers and carbonic anhydrase inhibitors) and/or increasing outflow facility (prostaglandin analogs, cholinergic agents). Among these drugs, prostaglandin F2α (PGF2α) analogs have become the first-line agents in treating open angle glaucoma because of their reliable intraocular pressure-lowering effect, good compliance (once daily application), and fewer side effects.
analogs approved for clinical application include latanoprost, bimatoprost, travoprost, as well as the recently developed tafluprost. PGF2α
analogs lower intraocular pressure by facilitating drainage of aqueous humor, predominantly through the uveoscleral outflow pathway, as well as to a lesser degree through the trabecular outflow pathway.5
It has been suggested that PGF2α
analogs bind to prostaglandin F receptors, activate signal transduction (probably via protein kinase C), and upregulate the expression of matrix metalloproteinases. All these biological changes lead to remodeling of the extracellular matrix, elevation in uveoscleral outflow facility, and controversial improvement in trabecular outflow facility.5