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Primary open-angle glaucoma (POAG) is one of the leading causes of blindness in the world. This optic neuropathy is characterized by an elevated intraocular pressure, which may be attributed to an increased resistence in the aqueous humor outflow pathways.
Histological studies have demonstrated that primary open-angle glaucoma is associated with pathological changes in the trabecular meshwork (TM).
Recent investigations have revealed an accumulation of aged cells in the outflow pathways of glaucomatous eyes as compared to age-matched control eyes. Glaucoma is characterized by increased oxidative stress-induced aging of trabecular meshwork cells, thus leading to elevated intraocular pressure. The goal of this study was to analyse the role of TGF-β2 in the induction of cellular aging in cultured human trabecular meshwork cells.