Cellular senescence, a characteristic feature of the aging process, is induced by diverse stressors. In recent years, glaucoma has emerged as a blinding ocular disease intricately linked to cellular senescence. The principal pathways implicated are oxidative stress, mitochondrial dysfunction, DNA damage, autophagy impairment, and the secretion of various senescence- associated secretory phenotype factors. Research on glaucoma-associated cellular senescence predominantly centers around the increased resistance of the aqueous humor outflow pathway, which is attributed to the senescence of the trabecular meshwork and Schlemm's canal. Additionally, it focuses on the mechanisms underlying retinal ganglion cell senescence in glaucoma and the corresponding intervention measures. Given that cell senescence represents an irreversible phase preceding cell death, an in-depth investigation into its mechanisms in the pathogenesis and progression of glaucoma, particularly by specifically blocking the signal transduction of cell senescence, holds the potential to decrease the outflow resistance of aqueous humor. This, in turn, could provide a novel avenue for safeguarding the optic nerve in glaucoma.