Although adenosine 5′-triphosphate (ATP) release from retinal neurons and astrocytes has been demonstrated in short-term increases in intraocular pressure (IOP); such as in aqueous humor of humans with primary acute angle closure glaucoma, the response in chronic IOP elevation was not yet demonstrated and this group set out to investigate this in three different chronic glaucoma models (Tg-MyocY437H mice, rats with hypertonic saline injection into episcleral veins and monkeys with laser photocoagulation to the trabecular meshwork). They found increased levels of ATP in vitreal humor of all three models. Although contamination of intracellular ATP from cell rupture can occur, the group proceeded to further confirm this rise by measuring NTPDase1; an ectoenzyme which dephosphorylates ATP. This paper makes a good start at supporting the purinergic signalling pathway disturbance is sustained in glaucoma, suggesting a longer target window may be available for therapeutic rescue.

Rat, mouse and primate models of chronic glaucoma show sustained elevation of extracellular ATP and altered purinergic signalling in the posterior eye.
Lu W, Hu H, Sevigny J, et al.
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Wai Siene Ng

University Hospital of Wales, Cardiff, UK.

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