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Abstract
Glucocorticoid (GC)-induced ocular hypertension and secondary iatrogenic open-angle
glaucoma are serious side effects of GC therapy. Its clinical presentation is similar
in many ways to primary open-angle glaucoma, including increased aqueous outflow resistance
and morphological and biochemical changes to the trabecular meshwork (TM). Therefore,
a large number of studies have examined the effects of GCs on TM cells and tissues.
GCs have diverse effects on the TM, altering TM cell functions, gene expression, extracellular
matrix metabolism, and cytoskeletal structure. Some or all of these effects may be
responsible for the increased outflow resistance associated with GC therapy. In contrast
to GCs, several different classes of steroids appear to lower IOP. Additional research
will help better define the molecular mechanisms responsible for GC-induced ocular
hypertension and steroid-induced IOP lowering activity.