Glaucoma is a neurodegenerative disease characterized by progressive and irreversible necrosis and apoptosis of retinal ganglion cells (RGCs). Deformation of the lamina cribrosa (LC) has been identified as a factor leading to damage to the optic nerve and capillaries passing through the LC, ultimately causing visual field defects and glaucoma development. Recent advancements in molecular biology, both domestically and internationally, have enabled a more comprehensive and in‑depth understanding of glaucoma pathogenesis. In the present review, the role of molecular signaling pathways associated with RGCs apoptosis, optic nerve protection and regeneration, and LC damage and remodeling in the development of glaucoma, are summarized and discussed. The insights provided herein may offer new targets and ideas for interventions and treatment strategies for glaucoma.