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.
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http://dx.doi.org/10.3892/mmr.2024.13207 | DOI Listing |
Glaucoma is a leading cause of irreversible blindness, often associated with elevated intraocular pressure (IOP) due to trabecular meshwork (TM) dysfunction. Diabetes mellitus (DM) is recognized as a significant risk factor for glaucoma; however, the molecular mechanisms through which hyperglycemia affects TM function remain unclear. This study investigated the impact of high glucose on gene expression in human TM (HTM) cells to uncover pathways that contribute to TM dysfunction and glaucoma pathogenesis under diabetic conditions.
View Article and Find Full Text PDFJ Mol Histol
December 2024
Department of Ophthalmology, First Affilliated Hospital, Heilongjiang University of Chinese Medicine, No.26 Heping Road, Xiangfang District, Harbin, 150000, China.
Chronic oxidative stress (COS) is related to the pathophysiology of the trabecular meshwork (TM) in glaucoma. MicroRNAs (miRNAs) have a key role in the oxidative stress-mediated glaucoma. This work investigated the function of miR-126-5p in human trabecular meshwork cells (TMCs) under chronic oxidative stress (COS).
View Article and Find Full Text PDFChin Med J (Engl)
December 2024
Guangzhou National Laboratory, Guangzhou International Bio Island, Guangzhou, Guangdong 510530, China.
Background: Retinal ganglion cell (RGC) death caused by acute ocular hypertension is an important characteristic of acute glaucoma. Receptor-interacting protein kinase 3 (RIPK3) that mediates necroptosis is a potential therapeutic target for RGC death. However, the current understanding of the targeting agents and mechanisms of RIPK3 in the treatment of glaucoma remains limited.
View Article and Find Full Text PDFMol Biotechnol
December 2024
Department of Ophthalmology, The Second People's Hospital of Jinan, Jinan, 250000, Shandong, China.
Glaucoma is a leading cause of irreversible blindness, with rising incidence globally. Effective treatment is challenging due to limited understanding of the disease mechanisms. Growth factor activity is crucial in glaucoma, with potential to reduce retinal ganglion cell (RGC) apoptosis and slow disease progression.
View Article and Find Full Text PDFJ Clin Med
November 2024
Institute for Research in Ophthalmology, Foundation for Ophthalmology Development, 60-836 Poznan, Poland.
Glaucoma is a leading cause of irreversible blindness worldwide. It leads to the progressive degeneration of retinal ganglion cells (RGCs), the axons of which form the optic nerve. Enormous RGC apoptosis causes a lack of transfer of visual information to the brain.
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