Co-Treatment With rhBMP-2 and Rapamycin Modulates Osteogenesis-Adipogenesis Balance to Enhance Aged Bone Regeneration.
He Z., Bai X., Xie F., Wang X., Zhang F., Yu Y.
Animal Study, published in Adv Sci (Weinh) (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
- Adv Sci (Weinh) (2026)
- Country
- Germany
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 41603595
- DOI
- 10.1002/advs.202521619
Abstract (original English)
Recombinant human bone morphogenetic protein 2 (rhBMP-2) is a well-established osteoinductive agent used in clinical practice. In this study, rhBMP-2 is found to exacerbate the imbalance between osteogenesis and adipogenesis in senescent bone marrow stromal cells (BMSCs), resulting in excess adipocytes (eADs) accumulation and a diminished osteogenic response. However, the role of eADs in age-related bone repair deficits remains unclear. Our findings indicate that eADs within the aged microenvironment contribute to impaired bone regeneration by promoting BMSC senescence and suppressing osteogenic differentiation. To address this issue, we investigated the feasibility of regulating the abnormal differentiation of senescent BMSCs to enhance aged bone regeneration. Based on this, a novel energy-supplying hydrogel system (PEGSN-PGA/rhBMP-2/Rapa, PBR) suitable for the aged regenerative microenvironment and with excellent bone integration performance is designed for local minimally invasive treatment of aged bone defects. This system effectively regulates the abnormal differentiation of senescent BMSCs, maintains the cell cycle process, and retains the regenerative potential for bone repair in the senescent microenvironment. This study presents a novel strategy for the treatment of rhBMP-2-mediated bone degenerative diseases and offers a pioneering perspective on the interplay among a
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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