ArticleBone research2025
Pharmacological inhibition of RAS pathway alleviates spine deformity in a mouse model of neurofibromatosis type 1.
Article in Bone research, 2025. 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
Neurofibromatosis type 1 (NF1) is a genetic disorder affecting 1 in 3 000 people due to heterozygous mutations in the NF1 gene. Patients with NF1 can develop multiple symptoms, such as neurofibromas, skin hyperpigmentation, and bone abnormalities, including tibial pseudarthrosis and spine deformity. Here, we aimed to elucidate the cellular origin and pathogenic mechanism of NF1 spine deformity. We explored the Prss56-Nf1 knockout (KO) mouse model that recapitulates neurofibromas and pseudarthrosis by carrying Nf1 gene inactivation in Prss56-expressing boundary cap cells, a neural crest subset, and their derivatives. Micro-CT analyses showed that Prss56-Nf1 KO mice exhibit spine deformity from 12 months of age, associated with vertebral anomalies reminiscent of patients with NF1. Fate mapping revealed a significant increase in OSX
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