Department of Medical Laboratory, Xindu District People's Hospital of Chengdu, Chengdu, Sichuan 610500, P.R. China.
Sichuan Provincial Key Laboratory for Genetic Disease, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, Sichuan 610072, P.R. China.
Mol Med Rep. 2024 May;29(5). doi: 10.3892/mmr.2024.13207. Epub 2024 Mar 22.
Glaucoma is a group of progressive optic nerve disorders characterized by the loss of retinal ganglion cells, a thinner retinal nerve fibre layer and cupping of the optic disk. Apoptosis is a physiological cell death process regulated by genes and plays a crucial role in maintaining tissue homeostasis, ensuring the natural development and immune defence of organisms. Apoptosis has been associated with glaucoma and inhibiting apoptosis by activating phosphatidylinositol 3-kinase‑protein kinase B or other medicines can rescue pathological changes in glaucoma. Due to the complex crosstalk of apoptosis pathways, the pathophysiological mechanism of apoptosis in glaucoma needs to be fully elucidated. The present review aimed to discuss the mechanism of cell apoptosis in glaucoma, improve the understanding of the pathophysiology of glaucoma, summarize new directions for the treatment of glaucoma and lay the foundation for new treatment strategies for glaucoma.
青光眼是一组以视网膜神经节细胞丢失、视网膜神经纤维层变薄和视盘凹陷为特征的进行性视神经病变。细胞凋亡是一种受基因调控的生理细胞死亡过程,在维持组织内稳态、确保生物的自然发育和免疫防御方面发挥着关键作用。细胞凋亡与青光眼有关,通过激活磷脂酰肌醇 3-激酶-蛋白激酶 B 或其他药物抑制细胞凋亡可以挽救青光眼的病变。由于细胞凋亡途径的复杂相互作用,需要充分阐明青光眼细胞凋亡的病理生理学机制。本综述旨在讨论青光眼细胞凋亡的机制,加深对青光眼病理生理学的认识,总结青光眼治疗的新方向,并为青光眼的新治疗策略奠定基础。