ArticleScientific reports2019
Responses of primary osteoblasts and osteoclasts from hemizygous β-globin knockout thalassemic mice with elevated plasma glucose to 1,25-dihydroxyvitamin D
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- Vildagliptin and Omarigliptin Differentially Bind to DPP-4 Homodimers and Modulate Osteoclast-Mediated Bone Resorption.Comprehensive Physiology · 2026Article
- Vitamin D Deficiency as a Debatable Modulator of Outcomes in Transfusion-Dependent Thalassemia; An Overview of the Latest Findings: A Narrative Review.Health science reports · 2025Article
- Exploring the bone marrow micro environment in thalassemia patients: potential therapeutic alternatives.Frontiers in immunology · 2024Review
- Article
- NIPA2 regulates osteoblast function by modulating mitophagy in type 2 diabetes osteoporosis.Scientific reports · 2020Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
β-thalassemia is often associated with hyperglycemia, osteoporosis and increased fracture risk. However, the underlying mechanisms of the thalassemia-associated bone loss remain unclear. It might result from abnormal activities of osteoblasts and osteoclasts, and perhaps prolonged exposure to high extracellular glucose. Herein, we determined the rate of duodenal calcium transport in hemizygous β-globin knockout thalassemic (BKO) mice. Their bones were collected for primary osteoblast and osteoclast culture. We found that BKO mice had lower calcium absorption than their wild-type (WT) littermates. Osteoblasts from BKO mice showed aberrant expression of osteoblast-specific genes, e.g., Runx2, alkaline phosphatase and osteocalcin, which could be partially restored by 1,25(OH)
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