Retinal fibrosis is a serious complication of diseases such as age-related macular degeneration and diabetic retinopathy, characterized by abnormal myofibroblast activity and excessive extracellular matrix deposition, leading to permanent visual impairment. The mechanisms of retinal fibrosis remain unclear and current treatments are not fully understood. The article examines the pathogenesis of fibrosis from the perspective of the neurovascular unit, with an emphasis on the roles of endothelial cells, pericytes and glial cells. Key fibrotic processes include epithelial-mesenchymal transition (EMT) as well as macrophage-pericyte-to-myofibroblast transitions (MMT/PMT). Analyzes molecular mechanisms regulating myofibroblast activation and extracellular matrix deposition. It concludes by outlining potential therapeutic targets for the treatment of retinal fibrosis.