Ekici Eren, Moghimi Sasan
T.R. (Republic of Turkey) Ministry of Health, Ankara Etlik City Hospital, Department of Ophthalmology, Ankara, Turkiye.
Hamilton Glaucoma Center, Shiley Eye Institute, Viterbi Family Department of Ophthalmology, University of California San Diego, La Jolla, CA, USA.
Mol Aspects Med. 2023 Oct 27;94:101223. doi: 10.1016/j.mam.2023.101223.
Glaucoma, a leading cause of irreversible blindness worldwide, is a spectrum of neurodegenerative diseases characterized by the gradual deterioration of retinal ganglion cells (RGCs) and optic neuropathy. With complex etiology, glaucoma's major risk factors include elevated intraocular pressure (IOP), advanced age, ethnicity, systemic vascular factors, and genetic predisposition. By 2040, glaucoma is expected to affect over 110 million individuals aged 40 to 80, posing a significant economic burden. Glaucoma can be classified into open-angle, angle-closure, and developmental subtypes, with primary and secondary forms. The disease often progresses silently, gradually impairing the visual field (VF) until it reaches an advanced stage. Understanding the abnormal functional changes associated with glaucoma at the tissue, cellular, molecular, and genetic levels is crucial for comprehending its pathogenesis. This review examines the published data from the past two decades to shed light on the biological mechanisms underlying glaucoma development. The most evident factors in the development of glaucomatous optic neuropathy include elevated IOP, aging, genetic influences, followed by impaired ocular blood flow regulation. These factors are interconnected processes that lead to optic nerve damage, compromised circulation, and structural changes in glial and connective tissues. Contributing factors involve extracellular matrix remodeling, excitotoxicity, nitric oxide, oxidative stress, and neuroinflammation. Ultimately, all types of glaucoma result in RGC dysfunction and loss, causing irreversible visual impairment. While our understanding of glaucoma pathogenesis is evolving, further research is crucial for a comprehensive understanding of glaucoma pathogenesis and the development of effective treatments.
青光眼是全球不可逆性失明的主要原因，是一系列神经退行性疾病，其特征是视网膜神经节细胞（RGCs）逐渐退化和视神经病变。由于病因复杂，青光眼的主要危险因素包括眼压升高（IOP）、高龄、种族、全身血管因素和遗传易感性。到2040年，预计青光眼将影响超过1.1亿40至80岁的人群，带来巨大的经济负担。青光眼可分为开角型、闭角型和发育型亚型，有原发性和继发性两种形式。该疾病通常悄然进展，逐渐损害视野（VF），直至发展到晚期。了解青光眼在组织、细胞、分子和基因水平上的异常功能变化对于理解其发病机制至关重要。本综述审视了过去二十年发表的数据，以阐明青光眼发生发展的生物学机制。青光眼性视神经病变发展中最明显的因素包括眼压升高、衰老、遗传影响，其次是眼部血流调节受损。这些因素相互关联，导致视神经损伤、循环受损以及神经胶质和结缔组织的结构变化。促成因素包括细胞外基质重塑、兴奋性毒性、一氧化氮、氧化应激和神经炎症。最终，所有类型的青光眼都会导致RGC功能障碍和丧失，造成不可逆的视力损害。虽然我们对青光眼发病机制的理解在不断发展，但进一步的研究对于全面理解青光眼发病机制和开发有效治疗方法至关重要。
