ArticlePloS one2012
Protective roles of DMP1 in high phosphate homeostasis.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- Recent Advances in the Role of Osteocytes in Orthodontic Tooth Movement.International journal of molecular sciences · 2025Review
- Multifaceted skeletal effects of sevelamer carbonate in a secondary hyperparathyroidism model.Endocrine · 2025Article
- Preclinical Rodent Models for Human Bone Disease, Including a Focus on Cortical Bone.Endocrine reviews · 2024Review
- Extracellular FeScientific reports · 2023Article
- Contributions of Resin Cast Etching to Visualising the Osteocyte Lacuno-Canalicular Network Architecture in Bone Biology and Tissue Engineering.Calcified tissue international · 2023Review
- Dentin Matrix Protein 1 Silencing Inhibits Phosphorus Utilization in Primary Cultured Tibial Osteoblasts of Broiler Chicks.Frontiers in veterinary science · 2022Article
- The Role of DMP1 in CKD-MBD.Current osteoporosis reports · 2021Review
- Bone and heart health in chronic kidney disease: role of dentin matrix protein 1.Current opinion in nephrology and hypertension · 2019Review
- DMP1 prevents osteocyte alterations, FGF23 elevation and left ventricular hypertrophy in mice with chronic kidney disease.Bone research · 2019Article
- Article
- Review
- Maturation of cortical bone suppresses periosteal osteoprogenitor proliferation in a paracrine manner.Journal of molecular histology · 2016Article
- Critical roles of periostin in the process of orthodontic tooth movement.European journal of orthodontics · 2016Article
- Hypophosphatemic rickets: revealing novel control points for phosphate homeostasis.Current osteoporosis reports · 2014Review
- Constitutive nuclear expression of dentin matrix protein 1 fails to rescue the Dmp1-null phenotype.The Journal of biological chemistry · 2014Article
- Article
- Dentin matrix protein 1 and phosphate homeostasis are critical for postnatal pulp, dentin and enamel formation.International journal of oral science · 2012Article
- Intrinsically disordered proteins and biomineralization.Matrix biology : journal of the International Society for Matrix BiologyReview
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
purposeDmp1 (dentin matrix protein1) null mice (Dmp1(-/-)) display hypophosphatemic rickets with a sharp increase in fibroblast growth factor 23 (FGF23). Disruption of Klotho (the obligatory co-receptor of FGF23) results in hyperphosphatemia with ectopic calcifications formed in blood vessels and kidneys. To determine the role of DMP1 in both a hyperphosphatemic environment and within the ectopic calcifications, we created Dmp1/Klotho compound deficient (Dmp1(-/-)kl/kl) mice. PROCEDURES: A combination of TUNEL, immunohistochemistry, TRAP, von Kossa, micro CT, bone histomorphometry, serum biochemistry and Scanning Electron Microscopy techniques were used to analyze the changes in blood vessels, kidney and bone for wild type control, Dmp1(-/-), Klotho deficient (kl/kl) and Dmp1(-/-)kl/kl animals.
findingsInterestingly, Dmp1(-/-)kl/kl mice show a dramatic improvement of rickets and an identical serum biochemical phenotype to kl/kl mice (extremely high FGF23, hyperphosphatemia and reduced parathyroid hormone (PTH) levels). Unexpectedly, Dmp1(-/-)kl/kl mice presented elevated levels of apoptosis in osteocytes, endothelial and vascular smooth muscle cells in small and large blood vessels, and within the kidney as well as dramatic increase in ectopic calcification in all these tissues, as compared to kl/kl.
conclusionThese findings suggest that DMP1 has an anti-apoptotic role in hyperphosphatemia. Discovering this novel protective role of DMP1 may have clinical relevance in protecting the cells from apoptosis in high-phosphate environments as observed in chronic kidney disease (CKD).
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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.