Glucocorticoid-induced ocular hypertension(GIOH)is a condition characterized by elevated intraocular pressure caused by glucocorticoids. The long-term presence of GIOH may lead to optic nerve damage and visual field defects, eventually progressing to glucocorticoid-induced glaucoma(GIG), which can potentially cause blindness. Glucocorticoids primarily exert their biological effects by mediating glucocorticoid receptor(GR), while also involving factors such as transforming growth factor(TGF)-β, Wnt, and Rho in the formation of GIOH. In-depth exploration of the pathological changes and related molecular mechanisms of the trabecular meshwork in GIOH provides an important theoretical basis for understanding the pathogenesis and treatment of GIOH. Therefore, this article provides a review of the pathological changes and molecular mechanisms of the trabecular meshwork in GIOH, aiming to provide a theoretical basis for further research on the pathological mechanisms and treatment of GIOH.