Abstract
Glaucoma is a heterogenous, chronic, progressive group of eye diseases, which results in irreversible loss of vision. There are several types of glaucoma, whereas the primary open-angle glaucoma (POAG) constitutes the most common type of glaucoma, accounting for three-quarters of all glaucoma cases. The pathological mechanisms leading to POAG pathogenesis are multifactorial and still poorly understood, but it is commonly known that significantly elevated intraocular pressure (IOP) plays a crucial role in POAG pathogenesis. Besides, genetic predisposition and aggregation of abrogated proteins within the endoplasmic reticulum (ER) lumen and subsequent activation of the protein kinase RNA-like endoplasmic reticulum kinase (PERK)-dependent unfolded protein response (UPR) signaling pathway may also constitute important factors for POAG pathogenesis at the molecular level. Glaucoma is commonly known as a ‘silent thief of sight’, as it remains asymptomatic until later stages, and thus its diagnosis is frequently delayed. Thereby, detailed knowledge about the glaucoma pathophysiology is necessary to develop both biochemical and genetic tests to improve its early diagnosis as well as develop a novel, ground-breaking treatment strategy, as currently used medical therapies against glaucoma are limited and may evoke numerous adverse side-effects in patients.
Highlights
Glaucoma is a chronic and progressive disease affecting the structures of the eye, leading to the optic nerve atrophy, to apoptosis of retinal ganglion cells (RGCs), and to loss of vision [1,2,3]
Pasquale et al have reported that alleles of CDKN2BAS1 single nucleotide polymorphisms, which influence the risk of developing primary open-angle glaucoma (POAG), may have a significant impact on optic nerve degeneration among POAG individuals, which indicates an important role of CDKN2BAS1 in POAG pathogenesis [202]
POAG, the most common form of the glaucoma, rarely causes symptoms until it is at the advanced stage, it is commonly known as a ‘silent thief of sight’
Summary
Glaucoma is a chronic and progressive disease affecting the structures of the eye, leading to the optic nerve atrophy, to apoptosis of retinal ganglion cells (RGCs), and to loss of vision [1,2,3]. Increased resistance to aqueous outflow via the TM is a characteristic of individuals with OAG, whereas in individuals with ACG, access to the drainage pathway is obstructed [10] Both OAG and ACG may constitute a primary disease [10], whereas a secondary glaucoma may develop inter alia as a result of trauma [11], intake of medications like corticosteroids [12,13], inflammation [14], or specific conditions such as pigment dispersion or pseudo-exfoliation [15,16,17]. It is commonly known that glaucoma development and progression are strictly correlated with the pathophysiology of the optic nerve, the rate and severity of which is affected by the level of IOP. It has been demonstrated that there is a high frequency of undiagnosed glaucoma cases worldwide, thereby many individuals that suffer from glaucoma are unaware about the disease progression [24,25,26,27,28]
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