Unraveling Key m6A Modification Regulators Signatures in Postmenopausal Osteoporosis through Bioinformatics and Experimental Verification
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View abstract on PubMed
Summary
This summary is machine-generated.YTH N6-methyladenosine RNA binding protein 3 (YTHDF3) is reduced in osteoporosis, impairing bone marrow mesenchymal stem cell function. Restoring YTHDF3 may enhance bone formation in osteoporosis patients.
Area Of Science
- Biomedical Science
- Molecular Biology
- Stem Cell Research
Background
- Bone marrow mesenchymal stem cells (BMSCs) are crucial for bone formation.
- Osteoporosis involves impaired osteogenic differentiation of BMSCs.
- The molecular mechanisms regulating osteogenic capacity in osteoporosis-derived BMSCs (OP-BMSCs) are not fully understood.
Purpose Of The Study
- To investigate the role of YTH N6-methyladenosine RNA binding protein 3 (YTHDF3) in OP-BMSCs.
- To identify YTHDF3 as a potential therapeutic target for enhancing bone formation in osteoporosis.
Main Methods
- Analysis of Gene Expression Omnibus (GEO) microarray datasets (GSE35956, GSE35958) to identify m6A regulators in osteoporosis.
- Differential expression, protein-protein interaction, and machine learning analyses to pinpoint key genes.
- Single-cell analysis, immune infiltration assessment, Mendelian randomization, in vivo, and in vitro experiments to validate findings.
Main Results
- YTHDF3 was identified as a critical hub gene associated with osteoporosis.
- YTHDF3 expression is significantly decreased in osteoporosis patient and mouse models.
- Silencing YTHDF3 in OP-BMSCs inhibited proliferation and osteogenic differentiation.
Conclusions
- YTHDF3 plays a significant role in the pathogenesis of osteoporosis.
- YTHDF3 regulates the proliferation and osteogenic differentiation of OP-BMSCs.
- Targeting YTHDF3 may offer a therapeutic strategy for osteoporosis.
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