ArticleWorld journal of stem cells2024
Unveiling the role of hypoxia-inducible factor 2alpha in osteoporosis: Implications for bone health.
Article in World journal of stem cells, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 3 citations in OpenAlex.
- GLP-1 regulates osteo-adipogenic fate of BMSCs via HIF-2-AKT signaling and supports trabecular bone in glucocorticoid-induced osteoporosis.Stem cell reports · 2026Article
- Review
- Bidirectional regulation factor of bone marrow mesenchymal stromal cells differentiation: a focus on bone-fat balance in osteoporosis.Stem cell research & therapy · 2025Review
- The role of hypoxic microenvironment in rheumatoid arthritis.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOsteoporosis (OP) has become a major public health problem worldwide. Most OP treatments are based on the inhibition of bone resorption, and it is necessary to identify additional treatments aimed at enhancing osteogenesis. In the bone marrow (BM) niche, bone mesenchymal stem cells (BMSCs) are exposed to a hypoxic environment. Recently, a few studies have demonstrated that hypoxia-inducible factor 2alpha (HIF-2α) is involved in BMSC osteogenic differentiation, but the molecular mechanism involved has not been determined.
aimTo investigate the effect of HIF-2α on the osteogenic and adipogenic differentiation of BMSCs and the hematopoietic function of hematopoietic stem cells (HSCs) in the BM niche on the progression of OP.
methodsMice with BMSC-specific HIF-2α knockout (Prx1-Cre;Hif-2α
resultsThe quantitative index determined by microcomputed tomography indicated that the femoral bone density of Prx1-Cre;Hif-2α
conclusionOur study showed that inhibition of HIF-2α decreases bone mass by inhibiting the osteogenic differentiation and increasing the adipogenic differentiation of BMSCs through inhibition of mTOR signaling in the BM niche.
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Registered trials
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