摘要：SummaryThe group of retinal degenerations, retinitis pigmentosa (RP), comprises more than 150 genetic abnormalities affecting photoreceptors. Finding degenerative pathways common to all genetic abnormalities may allow general treatment such as neuroprotection. Neuroprotection may include enhancing the function of cells that directly support photoreceptors, retinal pigment epithelial cells, and Müller glia. Treatment with fibroblast growth factor 21 (FGF21), a neuroprotectant, from postnatal week 4–10, during rod and cone loss in P23H mice (an RP model) with retinal degeneration, preserved photoreceptor function and normalized Müller glial cell morphology. Single-cell transcriptomics of retinal cells showed that FGF21 receptorFgfr1was specifically expressed in Müller glia/astrocytes. Of all retinal cells, FGF21 predominantly affected genes in Müller glia/astrocytes with increased expression of axon development and synapse formation pathway genes. Therefore, enhancing retinal glial axon and synapse formation with neurons may preserve retinal function in RP and may suggest a general therapeutic approach for retinal degenerative diseases.Graphical abstractDisplay OmittedHighlights•FGF21 restores retinal neuronal function and Müller glial cell morphology in mouse RP•Müller glial cells are the primary cells expressing FGF21 receptor in mouse retinas•FGF21 increases Müller glial axon development and synapse formation pathway genes•Synaptic connection between ONL and INL is preserved by FGF21Neuroscience; Cellular Neuroscience; Sensory Neuroscience
