The current research status of normal tension glaucoma

Abstract

Normal tension glaucoma (NTG) is a progressive optic neuropathy that mimics primary open-angle glaucoma, but lacks the findings of elevated intraocular pressure or other mitigating factors that can lead to optic neuropathy. The present review summarized the causes, genetics, and mechanisms underlying NTG in both animal models and human patients. We also proposed that the neurovascular unit is a therapeutic target for NTG management.

Keywords: aging; genetics; neurovascular unit; primary open-angle glaucoma; treatment.

Figure 1

Neurovascular dysfunction in the mechanism of NTG. Notes: Neurovascular unit is a collection of different cells around blood vessels – including neurons, glia cells, and vascular cells – forming a structural and functional integrated unit to maintain the normal balance of microenvironments. Neurovascular dysfunction includes the damage of BRBs, leading to the mal-transmission between blood vessels and the microenvironment around neurons. The damaging effects include extravasation, internal transportation of circulating toxin (ET-1, Aβ), release of inflammatory cytokines or antigens, etc, which will trigger retinal gliosis and lead to neural degeneration. Abbreviations: ET-1, endothelin-1; Aβ, amyloid-β; RGC, retinal ganglion cell; BRB, blood–retinal barrier; OBF, ocular blood flow; NTG, normal tension glaucoma.