ArticleDevelopment (Cambridge, England)2018
Molecular analysis of enthesopathy in a mouse model of hypophosphatemic rickets.
Article in Development (Cambridge, England), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 26 citations in OpenAlex.
- The PHEX deletion variant (p.Thr605MetfsTer14) causes X-linked hypophosphatemic rickets by reducing protein expression and promoting mineralization.Orphanet journal of rare diseases · 2026Article
- Diagnosis and Management of Hypophosphatemic Disorders.Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists · 2025Review
- Prevalence of enthesopathies in X-linked hypophosphatemia: an explorative ultrasound study.JBMR plus · 2025Article
- Review
- The role of GDF5 in regulating enthesopathy development in the Hyp mouse model of XLH.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2024Article
- Sclerostin modulates mineralization degree and stiffness profile in the fibrocartilaginous enthesis for mechanical tissue integrity.Frontiers in cell and developmental biology · 2024Article
- Impaired 1,25-dihydroxyvitamin D3 action underlies enthesopathy development in the Hyp mouse model of X-linked hypophosphatemia.JCI insight · 2023Article
- Engineered Decellularized Tendon Matrix Putty Preserves Native Tendon Bioactivity to Promote Cell Proliferation and Enthesis Repair.Journal of tissue engineering and regenerative medicine · 2023Article
- Musculoskeletal Comorbidities and Quality of Life in ENPP1-Deficient Adults and the Response of Enthesopathy to Enzyme Replacement Therapy in Murine Models.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022Article
- FGF23 signalling and physiology.Journal of molecular endocrinology · 2021Review
- Bi-fated tendon-to-bone attachment cells are regulated by shared enhancers and KLF transcription factors.eLife · 2021Article
- X-Linked Hypophosphatemia: A New Era in Management.Journal of the Endocrine Society · 2020Review
- Mineralized tissues in hypophosphatemic rickets.Pediatric nephrology (Berlin, Germany) · 2020Review
- Development of Enthesopathies and Joint Structural Damage in a Murine Model of X-Linked Hypophosphatemia.Frontiers in cell and developmental biology · 2020Article
- Loss and gain of bone in spondyloarthritis: what drives these opposing clinical features?Therapeutic advances in musculoskeletal disease · 2020Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
The bone tendon attachment site known as the enthesis comprises a transitional zone between bone and tendon, and plays an important role in enabling movement at this site. X-linked hypophosphatemia (XLH) is characterized by impaired activation of vitamin D, elevated serum FGF23 levels and low serum phosphate levels, which impair bone mineralization. Paradoxically, an important complication of XLH is mineralization of the enthesis (enthesopathy). Studies were undertaken to identify the cellular and molecular pathways important for normal post-natal enthesis maturation and to examine their role during the development of enthesopathy in mice with XLH (Hyp). The Achilles tendon entheses of Hyp mice demonstrate an expansion of hypertrophic-appearing chondrogenic cells by P14. Post-natally, cells in wild-type and Hyp entheses similarly descend from scleraxis- and Sox9-expressing progenitors; however, Hyp entheses exhibit an expansion of Sox9-expressing cells, and enhanced BMP and IHH signaling. These results support a role for enhanced BMP and IHH signaling in the development of enthesopathy in XLH.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.