Pathogenesis of Increased Intraocular Pressure in Primary Open‑Angle Glaucoma: Literature Review

Abstract

Introduction. Despite the high socio-economic significance of primary open-angle glaucoma (POAG), the etiotropic and pathogenetic treatment of this disorder has not yet been implemented, since the mechanisms of the development of this disease are not fully known and understood. One of the topical issues is the pathogenesis of ophthalmic hypertension in POAG.Purpose. To summarize the currently known mechanisms of ophthalmic hypertension in POAG to search for potential molecular targets for pathogenetic pharmacotherapy.Materials and methods. Analysis of publications on PubMed, Medline and eLibrary.Results. Ophthalmic hypertension in POAG emerges due to increased resistance to aqueous humor (AH) outflow. It is caused by increased stiffness of Schlemm’s canal endothelium and trabecular meshwork as a result of changes in the structure and biomechanical properties of its cells and extracellular matrix. These changes are determined by the interaction of signaling molecules in the form of a pathological circle, the main links of which are TGF-β2 and its receptor, Smad 2/3/4, YAP/TAZ, sFRP-1 and CTGF.Conclusion. The cause of ophthalmic hypertension in POAG is fibrosis of the trabecular meshwork. This pathological process is based on the interaction of proteins, the main of which are TGF-β2 and its receptor, Smad 2/3/4, YAP/TAZ, sFRP-1 and CTGF. These molecules can become promising targets for the pathogenetic pharmacological therapy of POAG.