ArticleMatrix biology : journal of the International Society for Matrix Biology
Sclerostin antibody (Scl-Ab) improves osteomalacia phenotype in dentin matrix protein 1(Dmp1) knockout mice with little impact on serum levels of phosphorus and FGF23.
Article in Matrix biology : journal of the International Society for Matrix Biology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- The vinculin-β-catenin axis promotes bone formation and repair: an essential prerequisite for the anti-osteoporotic efficacy of sclerostin-neutralizing antibody.Science China. Life sciences · 2026Article
- Τhe story of sclerostin inhibition: the past, the present, and the future.Hormones (Athens, Greece) · 2025Review
- Article
- Sclerostin antibody improves alveolar bone quality in the Hyp mouse model of X-linked hypophosphatemia (XLH).International journal of oral science · 2023Article
- GRP78 promotes the osteogenic and angiogenic response in periodontal ligament stem cells.European cells & materials · 2023Article
- Drug discovery of sclerostin inhibitors.Acta pharmaceutica Sinica. B · 2022Review
- Article
- Sclerostin Directly Stimulates Osteocyte Synthesis of Fibroblast Growth Factor-23.Calcified tissue international · 2021Article
- Osteoporosis Treatment with Anti-Sclerostin Antibodies-Mechanisms of Action and Clinical Application.Journal of clinical medicine · 2021Review
- Sclerostin-Neutralizing Antibody Treatment Rescues Negative Effects of Rosiglitazone on Mouse Bone Parameters.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2021Article
- Sclerostin Antibody Treatment Increases Bone Mass and Normalizes Circulating Phosphate Levels in Growing Hyp Mice.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2020Article
- High Fidelity of Mouse Models Mimicking Human Genetic Skeletal Disorders.Frontiers in endocrinology · 2019Review
- Impaired osteocyte maturation in the pathogenesis of renal osteodystrophy.Kidney international · 2018Article
- Role of the Wnt/International journal of endocrinology · 2018Review
- Osteocyte Protein Expression Is Altered in Low-Turnover Osteoporosis Caused by Mutations in WNT1 and PLS3.The Journal of clinical endocrinology and metabolism · 2017Article
- BMP1 and TLL1 Are Required for Maintaining Periodontal Homeostasis.Journal of dental research · 2017Article
- Review
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Unlike treatments for most rickets, the treatment using 1,25-(OH)2 vitamin D3 has little efficacy on patients with hypophosphatemic rickets, a set of rare genetic diseases. Thus, understanding the local cause for osteomalacia in hypophosphatemic rickets and developing an effective treatment to restore mineralization in this rare disease has been a longstanding goal in medicine. Here, we used Dmp1 knockout (KO) mice (whose mutations led to the same type of autosomal recessive hypophosphatemic rickets in humans) as the model in which the monoclonal antibody of sclerostin (Scl-Ab) was tested in two age groups for 8weeks: the prevention group (starting at age 4weeks) and the treatment group (starting at age 12weeks). Applications of Scl-Ab greatly improved the osteomalacia phenotype (>15%) and the biomechanical properties (3-point bending, ~60%) in the treated long-bone group. Our studies not only showed improvement of the osteomalacia in the alveolar bone, which has the highest bone metabolism rate, as well as the long bone phenotypes in treated mice. All these improvements attributed to the use of Scl-Ab are independent of the change in serum levels of phosphorus and FGF23, since Scl-Ab had little efficacy on those parameters. Finally, we propose a model to explain how Scl-Ab can improve the Dmp1 KO osteomalacia phenotype, in which the sclerostin level is already low.
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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.