About this Research Topic
Glial cells, non-neuronal cell types in the central nervous system (CNS), are essential for the development, maintenance and control of CNS functions. They have long been overlooked as only support cells, especially in ocular tissues. Increasing evidence support the importance of glial cells for proper ocular functions and their involvement in the pathogenesis of eye diseases such as glaucoma.
Glaucoma is a progressive optic neuropathy and the second leading cause of irreversible blindness worldwide. Retinal ganglion cells (RGCs) and their axons that converge to form the optic nerve are damaged early on in the disease and during glaucoma progression. Because RGCs are essential for transducing visual information to the brain, their dysfunction and death lead to visual impairment. An elevated intraocular pressure (IOP) is one of the major risk factors of glaucoma. While mechanical stress induced by an elevated IOP likely directly damage RGCs and the optic nerve, glaucoma can occur despite normal IOP. A significant percentage of glaucoma patients have IOP considered within normal limits (i.e. normal-tension glaucoma). Still other individuals tolerate elevated IOP without optic nerve injury. Therefore, we need to identify novel cellular and molecular targets independent of IOP in the pathogenesis of glaucoma.
Glial cells can be an attractive target for understanding glaucoma from a new perspective. Ocular glial cells can be divided into four types: astrocytes, Müller cells, oligodendrocytes and microglia. These cells reside in the retina, optic nerve head (ONH), and the optic nerve. The ONH shows excavation (i.e., “cupping”) resulting from tissue remodeling: the loss of prelaminar tissue including optic nerve axons and deformation of the posterior portion of the lamina cribrosa. Glial cells express a high number of genes implicated in tissue remodeling, which may initiate and hasten progression in glaucoma. In human glaucoma patients, the ONH glial cells become reactive and up-regulate neurotoxic molecules such as pro-inflammatory cytokines and reactive oxygen species. Studies using glaucoma animal models have demonstrated that blockade of neurotoxic glial cells protects RGCs and visual functions. These studies indicate that ocular glia can contribute to the pathogenesis of glaucoma.
This Research Topic aims to provide clinicians and researchers an opportunity to disseminate and highlight their original research and review articles focused on the potential roles of glia in glaucoma pathogenesis. This article collection will shed light on recent advances made in the field, provide direction and guidance to researchers, and fostering further research, thus contributing to the understanding of glaucoma and its management.
Glaucoma is a progressive optic neuropathy and the second leading cause of irreversible blindness worldwide. Retinal ganglion cells (RGCs) and their axons that converge to form the optic nerve are damaged early on in the disease and during glaucoma progression. Because RGCs are essential for transducing visual information to the brain, their dysfunction and death lead to visual impairment. An elevated intraocular pressure (IOP) is one of the major risk factors of glaucoma. While mechanical stress induced by an elevated IOP likely directly damage RGCs and the optic nerve, glaucoma can occur despite normal IOP. A significant percentage of glaucoma patients have IOP considered within normal limits (i.e. normal-tension glaucoma). Still other individuals tolerate elevated IOP without optic nerve injury. Therefore, we need to identify novel cellular and molecular targets independent of IOP in the pathogenesis of glaucoma.
Glial cells can be an attractive target for understanding glaucoma from a new perspective. Ocular glial cells can be divided into four types: astrocytes, Müller cells, oligodendrocytes and microglia. These cells reside in the retina, optic nerve head (ONH), and the optic nerve. The ONH shows excavation (i.e., “cupping”) resulting from tissue remodeling: the loss of prelaminar tissue including optic nerve axons and deformation of the posterior portion of the lamina cribrosa. Glial cells express a high number of genes implicated in tissue remodeling, which may initiate and hasten progression in glaucoma. In human glaucoma patients, the ONH glial cells become reactive and up-regulate neurotoxic molecules such as pro-inflammatory cytokines and reactive oxygen species. Studies using glaucoma animal models have demonstrated that blockade of neurotoxic glial cells protects RGCs and visual functions. These studies indicate that ocular glia can contribute to the pathogenesis of glaucoma.
This Research Topic aims to provide clinicians and researchers an opportunity to disseminate and highlight their original research and review articles focused on the potential roles of glia in glaucoma pathogenesis. This article collection will shed light on recent advances made in the field, provide direction and guidance to researchers, and fostering further research, thus contributing to the understanding of glaucoma and its management.
Keywords: Glaucoma, Glia, Neurodegeneration, Optic Nerve, Retina, Retinal Ganglion Cells
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