Impaired/dysfunctional aqueous collector channels may primarily contribute to the pathogenesis of primary open-angle glaucoma

Abstract

Primary open-angle glaucoma (POAG) is induced by elevated intraocular pressure (IOP) that arises due to increased resistance in conventional aqueous humor outflow pathway (AHOc) consisting of trabecular meshwork (TM), Schlemm’s canal (SC), and downstream vascular network including collector channels (CCs). Although it has been traditionally considered that most of the outflow resistance lies in TM and the inner wall of SC, recent studies identified that more than one third of the resistance lies on CCs and their connected vascular network. In addition, CCs draw more attention because minimally invasive glaucoma surgery (MIGS) whose success depends upon them has been recently spotlighted in the treatment of POAG. Despite the importance of CCs during the pathogenesis of POAG, glaucomatous changes in CCs of human patients have been only considered as secondary results without direct evidence due to the absence of glaucoma animal model primarily induced by CC impairment as well as difficulty in definitive visualization of AHOcin vivo. Here, we hypothesize that likewise in TM and SC inner wall, structural and functional impairment of CCs may also primarily contribute to the initiation and progression of POAG. This article introduces a potential strategy to investigate and treat CC-related POAG.