Posterior capsular opacification (PCO), a clouding of the lens capsule, can occur as a major complication after cataract surgery. The standard cataract surgical procedure involves the removal of the lens nucleus and cortex, while retaining a portion of the anterior capsule and the complete posterior capsule. Lens epithelial cells (LECs) are difficult to eliminate entirely, and the residual LECs are prone to proliferate and migrate, resulting in light scattering within the visual axis. Despite advancements in surgical interventions and intraocular lens (IOL) designs, PCO remains a widespread issue. The pathophysiological mechanisms underlying PCO primarily involve the proliferation, migration, and epithelial-mesenchymal transition (EMT) of residual LECs, which ultimately culminate in opacification of the posterior capsule. Recent years have witnessed substantial progress in elucidating the pathogenesis of PCO, facilitated by advancements in molecular biology techniques. This review summarizes current research on cellular and molecular mechanisms of PCO, focusing on LEC proliferation, migration, EMT, oxidative stress, extracellular matrix accumulation, and inflammation. Innovative therapeutic strategies, including IOL modifications, pharmacological interventions, and gene therapy, are being explored. Future research endeavors should concentrate on translating foundational research findings into clinical applications to enhance the prognosis for cataract patients.Copyright © 2025. Published by Elsevier Ltd.