ArticleJournal of pharmaceutical analysis2026
Mifepristone ameliorates osteoporosis & hyperlipidemia comorbidity through SPNS3-S1P-S1PR1 axis via regulating BMSCs differentiation.
Article in Journal of pharmaceutical analysis, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Osteoporosis (OP) and hyperlipidemia (HLP) are major public health concerns that often coexist in postmenopausal women due to ovarian senescence and metabolic dysregulation. This comorbidity drives bone marrow adipocyte accumulation and impaired osteoblast differentiation, linked to altered mesenchymal stem cell (BMSC) fate, thereby worsening both bone loss and lipid metabolic imbalance. However, the underlying mechanisms remain unclear. The purpose of this study was to identify key regulatory pathways underlying OP-HLP comorbidity and to explore potential therapeutic strategies targeting dysregulated BMSC differentiation. To investigate, we developed a murine OP-HLP comorbidity model by combining ovariectomy with a high-fat diet. BMSCs were induced under osteogenic or adipogenic conditions to assess differentiation patterns, while omics-based bioinformatics identified targets and pathways relevant to OP-HLP. Potential therapeutic agents were then screened virtually and validated experimentally. The results identified the SPNS lysolipid transporter 3 (SPNS3)-sphingosine-1-phosphate (S1P)-S1PR1 axis as a critical regulator of BMSCs differentiation. Mifepristone (MIF), acting as a structural stabilizer of SPNS3, enhanced osteogenic differentiation while inhibiting adipogenesis
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