TRIM27 Ubiquitinates and Degrades PPARγ to Promote Osteogenic Differentiation of BMSCs and Alleviate Osteoporosis
Liya Zhang, Junfeng Li, Benjuan Wu · 2026
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Description
Liya Zhang and co-authors identified a protein switch that tips stem cells toward making bone, with implications for osteoporosis. Their study appeared in the International Journal of Endocrinology in 2026. In bone marrow stem cells learning to become bone, levels of the protein TRIM27 more than doubled. Mice stripped of ovarian hormones, a standard model of postmenopausal bone loss, showed the opposite: TRIM27 fell as bones thinned.
Boosting TRIM27 in cells raised the hallmarks of bone building, from mineral deposits to bone marker genes, while silencing it stalled the process. The mechanism is targeted destruction: TRIM27 binds the fat-promoting regulator PPARγ and tags it for disposal, clearing a brake on bone formation. Knocking down that regulator rescued cells harmed by TRIM27 loss. In the mouse model, extra TRIM27 reduced bone loss. The authors nominate the pathway as a drug target for bone metabolism disorders.
Catalog record
| CREATOR | Liya Zhang, Junfeng Li, Benjuan Wu |
|---|---|
| YEAR | 2026 |
| COLLECTION | PAPERS |
| FORMAT | TXT |
| FILE SIZE | 24 KB |
| VERSION | 1.0 |
| LICENSE | CC BY 4.0 |
| RIGHTS | CC BY |
| SOURCE | Europe PMC |