ArticlePNAS nexus2026
Disease mechanisms revealed in the P23H opsin knock-in mouse model of retinitis pigmentosa.
Article in PNAS nexus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
The molecular mechanisms driving disease progression in autosomal dominant retinitis pigmentosa (adRP) due to a proline-to-histidine substitution (P23H) in opsin are not completely understood. Thus, we undertook to unlock features of the P23H/+ knock-in mouse model. Bisretinoids, the source of short-wavelength fundus autofluorescence (SW-AF), were elevated in albino P23H rhodopsin transgenic rats and in black and albino P23H/+ mice relative to wild type. Conversely, bisretinoid levels were lower in albino P23H/+ relative to black P23H/+ mice. Fluorescence microscopy revealed an inherent and aberrant autofluorescence in photoreceptor inner segments of albino P23H/+ mice. Outer nuclear layer (ONL) thinning indicative of photoreceptor degeneration was more pronounced in albino versus black P23H/+ mice and was accentuated in inferior versus superior hemiretina. Dark-rearing alleviated ONL thinning in albino P23H/+. The greatly diminished levels of ocular retinoid were not fully accounted for by loss of photoreceptor cells. P23H/+ mice treated with the antioxidant
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