ArticleNature genetics2006
Loss of DMP1 causes rickets and osteomalacia and identifies a role for osteocytes in mineral metabolism.
Article in Nature genetics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 577 papers, 1 of them a synthesis that pooled it.
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.
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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.
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Who cites it
577 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,191 citations in OpenAlex.
- X-linked hypophosphatemia and spinal cord compression: a systematic review and illustrative case.Acta neurochirurgica · 2026Pooled it
- FGF23 - A hormone produced by bone and has many faces.Reviews in endocrine & metabolic disorders · 2026Review
- When X Does Not Mark the Spot: Autosomal Dominant and Recessive Forms of Renal Hypophosphatemic Rickets and Osteomalacia.Current osteoporosis reports · 2026Review
- Article
- Fibroblast growth factor 23 at the crossroads of mineral metabolism and bone disease.Current opinion in nephrology and hypertension · 2026Review
- Hypophosphatemic rickets: diagnosis and treatment.Archives of endocrinology and metabolism · 2026Review
- Fibroblast growth factor 23: Regulation, signalling and systemic links between bone, metabolism and inflammation.Molecular metabolism · 2026Review
- Osteocyte Cell-Cell Communication Within and Beyond Bone.Current osteoporosis reports · 2026Review
- New knock-in mouse linesJBMR plus · 2026Article
- Expanding the Autosomal Recessive Hypophosphatemic Rickets Type I Carrier Phenotype and Adult Treatment with Burosumab.Calcified tissue international · 2026Article
- Bone matrix proteins: regulators of skeletal remodeling and repair.Journal of bone and mineral metabolism · 2026Review
- Genetic background of infantile hypophosphatemia: a narrative review.Translational pediatrics · 2026Review
- DMP1-Mediated FAK Activation Contributes to P Utilization of Broiler Osteoblasts by Suppressing FGF23 Expression.Biology · 2026Article
- Deep learning models to map osteocyte networks from confocal microscopy can successfully distinguish between young and aged bone.PLoS computational biology · 2026Article
- Pathomechanism of LYPD6 enhancing abnormal hyperostosis via Wnt/β-catenin signaling pathway in diffuse idiopathic skeletal hyperostosis.Journal of orthopaedic translation · 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
- Intravital Microscopy of Osteocytes: A New Era in Bone Cell Biology.Current osteoporosis reports · 2025Review
- Lunar life drives jawbone formation.Journal of dental sciences · 2025Article
- Recent Advances in the Role of Osteocytes in Orthodontic Tooth Movement.International journal of molecular sciences · 2025Review
- Multiscale Analysis Reveals Altered Characteristics in Femur and Mandible of Mice on a High Phosphate Diet.Calcified tissue international · 2025Article
517 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on byBone talk.2006
Authors and funding
15 authors at 6 institutions in 3 countries.
Funding
Abstract
The osteocyte, a terminally differentiated cell comprising 90%-95% of all bone cells, may have multiple functions, including acting as a mechanosensor in bone (re)modeling. Dentin matrix protein 1 (encoded by DMP1) is highly expressed in osteocytes and, when deleted in mice, results in a hypomineralized bone phenotype. We investigated the potential for this gene not only to direct skeletal mineralization but also to regulate phosphate (P(i)) homeostasis. Both Dmp1-null mice and individuals with a newly identified disorder, autosomal recessive hypophosphatemic rickets, manifest rickets and osteomalacia with isolated renal phosphate-wasting associated with elevated fibroblast growth factor 23 (FGF23) levels and normocalciuria. Mutational analyses showed that autosomal recessive hypophosphatemic rickets family carried a mutation affecting the DMP1 start codon, and a second family carried a 7-bp deletion disrupting the highly conserved DMP1 C terminus. Mechanistic studies using Dmp1-null mice demonstrated that absence of DMP1 results in defective osteocyte maturation and increased FGF23 expression, leading to pathological changes in bone mineralization. Our findings suggest a bone-renal axis that is central to guiding proper mineral metabolism.
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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.