Abstract: Glaucoma, an irreversible blinding eye disease characterized by optic nerve damage and visual field defects, has a pathogenesis closely linked to structural and functional alterations in the trabecular meshwork (TM) and Schlemm’s canal (SC). Integrins, serving as crucial transmembrane receptors on the cell surface, act as vital bridges connecting the extracellular matrix (ECM) to the cytoskeleton. Within the TM and SC, integrins exhibit subtype-specific distribution patterns. Through their modulation of cell-ECM adhesion, cytoskeletal reorganization, and cellular contractility, integrins critically influence TM tissue stiffness and the morphology/function of the aqueous humor outflow pathway. These roles suggest that targeting specific integrin subtypes—particularly αvβ3 and β1 subunits—may offer a promising strategy for modulating the pathological microenvironment in glaucoma.

Key words: Glaucoma, Trabecular meshwork, Integrin