Future Therapeutic Strategies in the Glaucoma Management

Abstract

Glaucoma is a group of eye diseases in which progressive damage to the ocular nerves may cause retinal ganglion cell (RGC) death. Worldwide glaucoma is a leading cause of avoidable blindness. Intraocular pressure (IOP) is considering to be the main identified cause of danger so far, and lowering intraocular pressure is the only recognized technique for inhibiting disease progression. Furthermore, blood vessels and genetic components of glaucoma are considered additional risk factors. In order to realize the potential progress of glaucoma treatment, new treatment strategies and ambitious goals are constantly being developing. These treatments will provide specific tissue goals to reduce IOP and ensure neuroprotective effects on RGCs. Consequently, physicians can shortly have an expanded range of medical choices to choose from, coupled with therapies that are more successful. Therefore, this study has reviewed the recent studies that were conducted on cellular mechanisms of glaucoma treatment.

The effect of Calcium channel blocker in the Betamethasone-induced Glaucoma model in rabbits

“…Inactivating calcium channel phosphorylation within the cell membrane, which occurs by inhibition of intracellular calcium absorption, will result in IOP reduction by CCBs [11]. It is well known that the shrinkage characteristics of the trabecular meshwork will be affected by the L-type Ca2 + channel.…”

“…The synthesis of extracellular matrix collagen protein may also be inhibited by CCBs, indicating beneficial effects on glaucoma [10]. CCB relaxes the trabecular meshwork cells by inhibiting the L-type channel located in the retina of the eye, thereby improving the outflow facilities of aqueous humor [11]. In the dissected eyes of humans, perfusion studies displayed a dose- related rise in the drainage facility later to topical CCBs administration [12].…”

The Effect of Levamlodipine in Glucose-Induced Acute Model of Glaucoma in Rabbits

“…The antihypertensive effect of levamlodipine is consistent with Waleed et al [31] demonstrated the hypotensive effect of topical nimodipine that follows administration and suggest the paramount role of levamlodipine in the regulation of IOP. Irina et al will strengthen this point, demonstrated the benefits of CCB in preventing the progression of adrenaline-induced acute glaucoma, especially in the early stages of the disease [13], [14]. There is a close interaction between Ca++ and adenylyl cyclase (AC) [15].…”

“…Verapamil causes permeability of the cell epithelium that inhibiting the formation of AH [25]. Changes in cAMP content in the ciliary zone also affect IOP by enhancing outflow facilities or inhibiting the formation of AH [14].…”

The Effect of Anabasis articulata Stems Extract on Lowering Intraocular Pressure in the Glaucoma Rat Model(Conference Paper )#

“…Herbal medicines have grown in importance as a subject of study for health care around the world (9) . Anabasis articulata (AA), also known as Ajrem, Eshnan, or Berry Bearing Glasswort, is a desert plant found in Iraq, Algeria, Syria, and Egypt.…”