Sildenafil suppresses osteoporosis-related bone marrow adiposity by inhibiting Adipogenic differentiation of mesenchymal stem cells.
Wu L., Hu M., Wei E., Pan X., Zhu Q., Wu T.
Animal Study, published in Cell Signal (2026) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Cell Signal (2026)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 41985733
- DOI
- 10.1016/j.cellsig.2026.112539
Abstract (original English)
Within the bone marrow niche, maintaining equilibrium between mesenchymal stem cell (MSC) commitment toward osteoblasts and adipocytes is essential for preserving tissue homeostasis. Excessive adipogenic differentiation of MSCs contributes to disorders such as osteoporosis. Targeting marrow adiposity, alongside promoting osteogenesis, may offer a promising therapeutic approach. Sildenafil, a U.S. Food and Drug Administration-approved drug, has been suggested to influence cellular differentiation; however, its potential role in regulating adipogenic differentiation of MSCs remains unclear. Here, we investigated its regulatory effects on MSC adipogenic conversion and bone marrow fat accumulation under osteoporotic conditions, as well as its underlying mechanisms. Adipogenic differentiation of human MSCs (hMSCs)-specifically human adipose-derived MSCs (hASCs) and human bone marrow-derived MSCs (hBMSCs)-was assessed by Oil Red O staining, quantitative reverse transcription polymerase chain reaction, and immunofluorescence. In vivo effects were evaluated using an ectopic adipogenesis model in nude mice and two osteoporotic mouse models (ovariectomized and tail-suspension models). RNA sequencing was performed for mechanistic analysis, followed by experimental validation. Sildenafil significantly inhibited adipogenic differentiation of hMSCs in vitro, suppressed adipogenesis of hBMSCs
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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