Glaucoma: from pathogenic mechanisms to retinal glial cell response to damage

Glaucoma: from pathogenic mechanisms to retinal glial cell response to damage

25 January 2024 | Jose A. Fernández-Albarral, Ana I. Ramírez, Rosa de Hoz, José A. Matamoros, Elena Salobrar-García, Lorena Elvira-Hurtado, Inés López-Cuenca, Lidia Sánchez-Puebla, Juan J. Salazar, and José M. Ramírez
Glaucoma is a neurodegenerative disease characterized by irreversible loss of retinal ganglion cells (RGCs) and visual impairment. The main events in its pathogenesis include degeneration and loss of RGC axons, as well as damage and remodeling of the lamina cribrosa. Elevated intraocular pressure (IOP) is a significant risk factor, but it is not the sole trigger, as other factors such as age, ocular biomechanics, and low ocular perfusion pressure also play roles. The neurodegenerative process involves ischemia/hypoxia, mitochondrial dysfunction, oxidative stress, and neuroinflammation. Glial cells, including microglia, astrocytes, and Müller cells, are involved in immunoregulation and their activation can lead to a proinflammatory state, disrupting the blood-retinal barrier and contributing to RGC death. MicroRNAs (miRNAs) are involved in various pathways related to glaucoma, including apoptosis, autophagy, neurogenesis, and oxidative stress. Genetic factors, such as mutations in genes like MYOC, OPTN, and TBK1, also contribute to the disease. Neuroinflammation, characterized by glial cell activation and the release of proinflammatory cytokines, is a key factor in glaucoma progression. The activation of glial cells can lead to a neurotoxic response, exacerbating neuronal damage and contributing to the overall pathology of the disease.Glaucoma is a neurodegenerative disease characterized by irreversible loss of retinal ganglion cells (RGCs) and visual impairment. The main events in its pathogenesis include degeneration and loss of RGC axons, as well as damage and remodeling of the lamina cribrosa. Elevated intraocular pressure (IOP) is a significant risk factor, but it is not the sole trigger, as other factors such as age, ocular biomechanics, and low ocular perfusion pressure also play roles. The neurodegenerative process involves ischemia/hypoxia, mitochondrial dysfunction, oxidative stress, and neuroinflammation. Glial cells, including microglia, astrocytes, and Müller cells, are involved in immunoregulation and their activation can lead to a proinflammatory state, disrupting the blood-retinal barrier and contributing to RGC death. MicroRNAs (miRNAs) are involved in various pathways related to glaucoma, including apoptosis, autophagy, neurogenesis, and oxidative stress. Genetic factors, such as mutations in genes like MYOC, OPTN, and TBK1, also contribute to the disease. Neuroinflammation, characterized by glial cell activation and the release of proinflammatory cytokines, is a key factor in glaucoma progression. The activation of glial cells can lead to a neurotoxic response, exacerbating neuronal damage and contributing to the overall pathology of the disease.
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[slides and audio] Glaucoma%3A from pathogenic mechanisms to retinal glial cell response to damage