glazmagThe EYE ГЛАЗThe EYE GLAZ2222-44082686-8083Академия медицинской оптики и оптометрии10.33791/2222-4408-2021-4-23-30glazmag-244Research ArticleОБЗОР ЛИТЕРАТУРЫREVIEWSПатогенез увеличения внутриглазного давления при первичной открытоугольной глаукоме: обзор литературыPathogenesis of Increased Intraocular Pressure in Primary Open‑Angle Glaucoma: Literature Reviewhttps://orcid.org/0000-0002-2547-5913ПановА. А.PanovA. A.

Панов Андрей Алексеевич, студент факультета фундаментальной медицины

119991, Москва, Ломоносовский проспект, д. 27, корп. 1

Andrey A. Panov, student of the Faculty of Fundamental Medicine

27/1, Lomonosovsky Ave., Moscow, 119991

andrew_pan98@mail.ruАкопянВ. С.AkopyanV. S.

Акопян Владимир Сергеевич, доктор медицинских наук, профессор, заведующий кафедрой офтальмологии факультета фундаментальной медицины

119991, Москва, Ломоносовский проспект, д. 27, корп. 1

Vladimir S. Akopyan, Dr. Sci. (Med.), Professor, chairman of department of ophthalmology, Faculty of Fundamental Medicine

27/1, Lomonosovsky Ave., Moscow, 119991

akopyan_vs@yahoo.comhttps://orcid.org/0000-0002-7928-5410СеменоваН. С.SemenovaN. S.

Семенова Наталия Сергеевна, кандидат медицинских наук, доцент кафедры офтальмологии факультета фундаментальной медицины

119991, Москва, Ломоносовский проспект, д. 27, корп. 1

Nataliya S. Semenova, Cand. Sci. (Med.), Associate professor of department of ophthalmology, Faculty of Fundamental Medicine

27/1, Lomonosovsky Ave., Moscow, 119991

semenovans@gmail.comФГБОУ ВО «Московский государственный университет имени М.В. Ломоносова»РоссияLomonosov Moscow State UniversityRussian Federation2021121220212342330Copyright © Академия медицинской оптики и оптометрии, 20212021Академия медицинской оптики и оптометрииАкадемия медицинской оптики и оптометрииhttps://www.theeyeglaz.com/jour/about/submissions#copyrightNoticehttps://www.theeyeglaz.com/jour/article/view/244Введение

Введение. Несмотря на высокую социально-экономическую значимость первичной открытоугольной глаукомы (ПОУГ), до сих пор не разработано этиотропное и патогенетическое лечение этой болезни, поскольку не до конца известны и понятны механизмы развития данного заболевания. Одним из актуальных вопросов остается патогенез офтальмогипертензии при ПОУГ.

Цель

Цель. Обобщить известные на сегодня механизмы развития офтальмогипертензии при ПОУГ с целью поиска молекулярных мишеней для патогенетической фармакотерапии.

Методы исследования

Методы исследования. Анализ публикаций на ресурсах PubMed, Medline и eLibrary.

Результаты

Результаты. Офтальмогипертензия при ПОУГ возникает вследствие увеличения сопротивления оттоку внутриглазной жидкости (ВГЖ). Причиной этому может служить повышение жесткости эндотелия Шлеммова канала и трабекулярной сети в результате изменения структуры и биомеханических свойств ее клеток и внеклеточного матрикса. Эти изменения обусловлены взаимодействием между собой сигнальных молекул в виде патологического круга, основными звеньями которого являются TGF-β2 и его рецептор, Smad 2/3/4, YAP/TAZ, sFRP-1 и CTGF.

Заключение

Заключение. Причиной офтальмогипертензии при ПОУГ является фиброз трабекулярной сети. В основе данного патологического процесса лежит взаимодействие белков, основными из которых являются TGF-β2 и его рецептор, Smad 2/3/4, YAP/TAZ, sFRP-1 и CTGF. Эти молекулы могут стать перспективными мишенями для патогенетической фармакотерапии ПОУГ.

Introduction

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

Purpose. To summarize the currently known mechanisms of ophthalmic hypertension in POAG to search for potential molecular targets for pathogenetic pharmacotherapy.

Materials and methods

Materials and methods. Analysis of publications on PubMed, Medline and eLibrary.

Results

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

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.

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The authors declare that there are no conflicts of interest present.