ArticleJournal of orthopaedic translation2025
Fibroblast growth factor receptor 3 mutation promotes HSPB6-mediated cuproptosis in hypochondroplasia by impairing chondrocyte autophagy.
Article in Journal of orthopaedic translation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Growth plate cartilage-targeting nanoparticles for pharmacological treatment of hypochondroplasia.Bioactive materials · 2026Article
- Mitochondrial convergence of ferroptosis and cuproptosis in castration-resistant prostate cancer: From metabolic vulnerabilities to therapeutic targeting.BBA advances · 2026Review
- Mechanisms and therapeutic strategies of copper homeostasis in the pathogenesis of sepsis-induced cardiomyopathy.Frontiers in cell and developmental biology · 2026Review
- Tackling musculoskeletal disorders in an aging world: Advances in orthopaedic translational research.Journal of orthopaedic translation · 2025Article
- [Growth plate regulation and short stature: mechanistic insights and therapeutic advances].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatricsReview
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Hypochondroplasia (HCH) is a prevalent form of dwarfism linked to mutations in the fibroblast growth factor receptor 3 ( Methods: We generated an Results: We observed that Conclusions: Our study provides the first evidence for the pathogenicity of a gain-of-function mutation in Translational potential of this article: We first demonstrate that impaired autophagy and enhanced cuproptosis are pivotal in the pathogenesis of HCH. This study not only enlarged the therapeutic potential of targeting cuproptosis for treating
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Registered trials
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