Autophagy is a self-digestive process in which cellular components are degraded and recycled to maintain homeostasis and cope with stress. When cells are in a state of stress, autophagy will degrade proteins, lipids and damaged organelles, and convert them into key nutrients and building cornerstones needed to maintain cell homeosis. More and more evidence shows that there is a link between autophagy process damage and the development of a variety of ophthalmic diseases that seriously threaten vision, including age-related macular degeneration, glaucoma and the formation of cataracts. Through a systematic review, we integrate experimental data covering basic biological mechanisms, genetic models and clinical evidence to clarify these pathological associations. With a focus on the mechanisms and regulation of autophagy in various ocular tissues and diseases, we analyzed research on autophagy in the lens, retina, cornea, and trabecular meshwork. Key findings elucidate the specific mechanisms of autophagy in maintaining lens transparency, promoting retinal ganglion cell survival, and regulating ocular immunity, demonstrating its critical role in preserving cellular equilibrium in ocular tissues. Furthermore, we evaluated potential therapeutic strategies targeting autophagic pathways, including mammalian target of rapamycin (mTOR) inhibition, transcription factor EB(TFEB) activation, noncoding RNA regulation, gene editing, and artificial intelligence-assisted diagnostics, which show significant promise for modulating autophagy to treat ocular diseases. The results of this review underscore the importance of autophagy in ocular health and disease.