ArticleScientific reports2016
Senescence: novel insight into DLX3 mutations leading to enhanced bone formation in Tricho-Dento-Osseous syndrome.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- Craniofacial syndromes and class III phenotype: common genotype fingerprints? A scoping review and meta-analysis.Pediatric research · 2024Pooled it
- Suppression of distal-less homeobox 3 increased alveolar bone mass in mouse tooth socket by targeting thrombospondin 1.Journal of dental sciences · 2026Article
- Expression ofInternational journal of molecular sciences · 2025Article
- Cell signaling and transcriptional regulation of osteoblast lineage commitment, differentiation, bone formation, and homeostasis.Cell discovery · 2024Review
- DLX3 (Q178R) mutation delays osteogenic differentiation via H19/miR-29c-3p/KDM5B axis in TDO-iPSCs-derived MSCs.Genes & diseases · 2024Article
- MAST4 regulates stem cell maintenance with DLX3 for epithelial development and amelogenesis.Experimental & molecular medicine · 2024Article
- New Understandings from the Biophysical Study of the Structure, Dynamics, and Function of Nucleic Acids 2.0.International journal of molecular sciences · 2022Article
- Temporal Modulation of DNA Methylation and Gene Expression in Monolayer and 3D Spheroids of Dental Pulp Stem Cells during Osteogenic Differentiation: A Comparative Study.Tissue engineering and regenerative medicine · 2022Article
- Salt Dependence of DNA Binding Activity of Human Transcription Factor Dlx3.International journal of molecular sciences · 2022Article
- Dental management of tricho-dento-osseous syndrome in adolescent patients: Literature review and case presentation.Dental research journal · 2021Article
- The miR-4739/DLX3 Axis Modulates Bone Marrow-Derived Mesenchymal Stem Cell (BMSC) Osteogenesis Affecting Osteoporosis Progression.Frontiers in endocrinology · 2021Article
- Human Genetics of Sclerosing Bone Disorders.Current osteoporosis reports · 2018Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
The homeodomain transcription factor distal-less homeobox 3 gene (DLX3) is required for hair, tooth and skeletal development. DLX3 mutations have been found to be responsible for Tricho-Dento-Osseous (TDO) syndrome, characterized by kinky hair, thin-pitted enamel and increased bone density. Here we show that the DLX3 mutation (c.533 A>G; Q178R) attenuates osteogenic potential and senescence of bone mesenchymal stem cells (BMSCs) isolated from a TDO patient, providing a molecular explanation for abnormal increased bone density. Both DLX3 mutations (c.533 A>G and c.571_574delGGGG) delayed cellular senescence when they were introduced into pre-osteoblastic cells MC3T3-E1. Furthermore, the attenuated skeletal aging and bone loss in DLX3 (Q178R) transgenic mice not only reconfirmed that DLX3 mutation (Q178R) delayed cellular senescence, but also prevented aging-mediated bone loss. Taken together, these results indicate that DLX3 mutations act as a loss of function in senescence. The delayed senescence of BMSCs leads to increased bone formation by compensating decreased osteogenic potentials with more generations and extended functional lifespan. Our findings in the rare human genetic disease unravel a novel mechanism of DLX3 involving the senescence regulation of bone formation.
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Registered trials
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