Abstract
AbstractGlaucoma is the second leading cause of irreversible blindness worldwide, thought to affect 60 million people. It is a chronic progressive optic neuropathy with characteristic changes in the optic nerve head and subsequent visual field defects. In glaucoma, the lamina cribrosa (LC) region undergoes thickening and posterior migration in the early stages of the disease process, and later undergoes shearing and collapse of the LC plates leading finally to a thin fibrotic connective tissue structure/scar. This is characterised by the build‐up of extracellular matrix material and it is thought that this accumulation eventually results in elevated intraocular pressure and subsequent nerve damage. Here, we directly address the ongoing fibrotic pathology by use of alpha‐smooth actin expressing (myofibroblast‐like) human primary LC cells, including mechanisms of fibrosis and potential anti‐fibrotic therapies. Additionally we discuss the potential role of the Retinal Pigment Epithelial cell as a mediator of glaucomatous optic disc cupping / fibrosis through epithelial to mesenchymal transition.
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