Introduction. Ocular inflammation has emerged as a prominent subject in the realm of ophthalmology, engaging multiple medical domains, including internal medicine, surgery, basic research, physiology, pharmacology, microbiology, immunology, rheumatology, and laboratory investigations. Cytokine is a general term used for small secreted proteins that are key modulators of inflammation. They are produced in response to invading pathogens to stimulate, recruit, and proliferate immune cells. Purpose. To comprehend the ethiopathogenetic mechanisms underlying ocular inflammation and discover innovative approaches for its treatment. Epidemiology. Among uveitic patients, 10 to 46% experience elevated intraocular pressure. Uveitic glaucoma manifests in 20% of these cases, typically observed in individuals with chronic uveitis, with Posner-Schlossman syndrome, Fuch's heterochromic iridocyclitis, or uveitis associated with herpes simplex virus or varicella-zoster virus. Discussions. Exploring ocular inflammation within the framework of etiopathogenetic mechanisms proves promising for global advancements in ophthalmology. The administration of intraocular therapy holds the potential to attenuate the levels of proin-flammatory cytokines, thereby contributing to the amelioration and slowdown of ocular deterioration. The dysregulation between the formation and drainage of aqueous humor, prompted by inflammation, results in elevated intraocular pressure (IOP). In the context of anterior uveitis or panuveitis, inflammation directly impacts the drainage pathways of aqueous humor, leading to increased IOP and the development of glaucoma as a complication. Persistent intraocular inflammation triggers heightened production of inflamma-tory cytokines, including IL-1β and IL-6, stimulating Muller cells to generate VEGF. VEGF, in turn, exacerbates the inflammatory response by enhancing vascular permeability and contributing to the disruption of the blood-retinal barrier.