Abstract
Glaucoma is a progressive optic neuropathy characterized by visual field defects that ultimately lead to irreversible blindness (Alward, 2000; Anderson et al., 2006). By the year 2020, an estimated 80 million people will have glaucoma, 11 million of which will be bilaterally blind. Primary open-angle glaucoma (POAG) is the most common type of glaucoma. Elevated intraocular pressure (IOP) is currently the only risk factor amenable to treatment. How IOP is regulated and can be modulated remains a topic of active investigation. Available therapies, mostly geared toward lowering IOP, offer incomplete protection, and POAG often goes undetected until irreparable damage has been done, highlighting the need for novel therapeutic approaches, drug targets, and biomarkers (Heijl et al., 2002; Quigley, 2011). In this review, the role of soluble (nitric oxide (NO)-activated) and membrane-bound, natriuretic peptide (NP)-activated guanylate cyclases that generate the secondary signaling molecule cyclic guanosine monophosphate (cGMP) in the regulation of IOP and in the pathophysiology of POAG will be discussed.
Highlights
Glaucoma is a progressive optic neuropathy characterized by visual field defects that lead to irreversible blindness (Alward, 2000; Anderson et al, 2006)
There is no definitive cure for Primary open-angle glaucoma (POAG) and multiple risk factors for POAG have been identified [including intra-ocular pressure (IOP), race, age, and genetic factors], the molecular signaling involved in POAG pathogenesis remains largely unknown
There continues to be an urgent need for biomarkers that allow to detect/diagnose/track POAG progression and treatment efficacy
Summary
The existence of a third outflow route was postulated: lymphatic channels in the stroma of the ciliary body and interstitial spaces between CM muscle bundles may function as a backup outflow system (Yucel et al, 2009) The relevance of this uveolymphatic pathway and whether NO-cGMP signaling (see “NO-cGMP signaling in the eye” below) modulates contractility of ocular lymphatic vessels remains to be determined. The idea that vascular dysfunction contributes to the pathogenesis of POAG is based on the hypothesis that decreased perfusion of the optic nerve leads to neurodegeneration (Harris et al, 2005; Vajaranant and Pasquale, 2012) Both impaired blood flow and impaired vascular autoregulation have been described in glaucoma patients (Flammer et al, 2002; Feke and Pasquale, 2008; Moore et al, 2008; Feke et al, 2011). Both an NO donor and a cGMP-analog decreased IOP (Kotikoski et al, 2002) and increased outflow facility in rabbits
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