Retinal glial cells, including Müller cells, astrocytes, and microglia, are the core cell populations maintaining retinal homeostasis. Under physiological conditions, glial cells ensure the structural and functional integrity of neurons by regulating ion balance, providing neurotrophic support, participating in synaptic pruning, and modulating the neurovascular unit. During the progression of retinitis pigmentosa (RP), the functional states of glial cells undergo significant pathological changes: Müller cells exhibit reactive gliosis, metabolic dysregulation, and glial scar formation, disrupting the retinal laminar structure; astrocytes undergo phenotypic transformation and vascular remodeling, compromising the blood-retinal barrier; microglia evolve into a disease-associated phenotype and migrate to the outer retina. While clearing debris, microglia trigger aberrant phagocytosis of surviving photoreceptors due to the dysregulation of the CD47-SIRPα signaling pathway, thereby accelerating neurodegeneration. The imbalanced crosstalk among these glial cells collectively drives the pathological remodeling in RP. Current glia-targeted therapeutic strategies, such as utilizing Müller cells for neurotrophic factor delivery or cellular regeneration, and modulating microglial activity to suppress neuroinflammation, demonstrate clinical potential in delaying visual function loss, providing a new theoretical basis and therapeutic window for the comprehensive intervention of RP.
