KATP Channel Activation by Statins Decreases Intra-Ocular Pressure. Should We Explore These Channels as Therapeutic Targets in Glaucoma?

Introduction: This review discusses the molecular mechanisms responsible for the normalization of otherwise raised intraocular pressure (IOP) in patients of glaucoma when they are administered statin therapy. Material and Methods: Literature published between 1990 and 2016 on the pathophysiology of glaucoma and the action of statins has been reviewed. Data Synthesis: A decrease in resistance to aqueous humor flow through trabecular meshwork (TM) in the eye tissue results in lessening of the raised intraocular pressure. KATP channels have been discovered in the eye tissue recently. Activation of KATP channels facilitates the flow of aqueous humor through the TM. This presumption is strengthened by the action of statins. Statins activate these KATP channels and, thereby, facilitate the aqueous flow through TM leading to relief in IOP. Statins interfere in the cholesterol biosynthesis pathway leading to decreased cholesterol synthesis. However, a simultaneous decrease in the level of ubiquinone leads to activation of KATP channels. Further, accumulation of LC Acetyl CoAs also activates these KATP channels. Expert Opinion: Statins decrease the elevated intraocular pressure in glaucoma by activating KATP channels. KATP channels are recently discovered therapeutic targets which may be exploited in the treatment of glaucoma.