
In glaucoma, regardless of its etiology, retinal ganglion cells degenerate and eventually die. Although age and elevated intraocular pressure (IOP) are the main risk factors, there are still many mysteries in the pathogenesis of glaucoma. The advent of genome-wide microarray expression screening together with the availability of animal models of the disease has allowed analysis of differential gene expression in all parts of the eye in glaucoma. This review will outline the findings of recent genome-wide expression studies and discuss their commonalities and differences. A common finding was the differential regulation of genes involved in inflammation and immunity, including the complement system and the cytokines transforming growth factor β (TGFβ) and tumor necrosis factor α (TNFα). Other genes of interest have roles in the extracellular matrix, cell-matrix interactions and adhesion, the cell cycle, and the endothelin system.
Retinal Ganglion Cells, Tumor Necrosis Factor-alpha, Optic Disk, Gene Expression, Glaucoma, Complement System Proteins, Disease Models, Animal, Mice, Transforming Growth Factor beta, Animals, Humans, Genome-Wide Association Study
Retinal Ganglion Cells, Tumor Necrosis Factor-alpha, Optic Disk, Gene Expression, Glaucoma, Complement System Proteins, Disease Models, Animal, Mice, Transforming Growth Factor beta, Animals, Humans, Genome-Wide Association Study
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