How RBP-J controls bone loss in arthritis
Official title: Regulation of Osteoclastogenesis and Arthritic Bone Resorption by RBP-J
Funded at Hospital for Special Surgery · NIH-11249529 · Data updated 2026-11-12
This work aims to understand how the protein RBP-J and the enzyme Hs2st1 control inflammation-driven bone loss in people with rheumatoid arthritis.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Hospital for Special Surgery NIH-funded |
| Lab location | 1 site (New York, UNITED STATES) |
| Project start | April 1, 2017 |
| Project end | December 31, 2028 |
| Funding year | 2026 |
| Award (this year) | $619,887 |
| NIH project number | 5R01AR071463-08 |
| Project ID | NIH-11249529 on NIH RePORTER |
Who could benefit from this research
✓Could help
People with rheumatoid arthritis who have active inflammatory bone erosion or high TNF-driven inflammation would be most relevant to this work.
✕Less likely to help
People with non-inflammatory bone loss (for example age-related osteoporosis) or those seeking immediate treatment options are unlikely to benefit directly from this preclinical research.
What this research studies
If you have rheumatoid arthritis, this project studies why inflammation causes bone erosion and how that process might be stopped. Researchers focus on osteoclasts (the bone cells that break down bone) and on TNF-driven pathways that cause inflammatory bone loss. Lab and animal experiments are used to trace how the transcriptional repressor RBP-J limits TNF-induced osteoclast formation and to test Hs2st1 as a downstream mediator. Findings may be compared with human cells or tissue samples to link the lab results back to patients.
Why it matters
Potential benefit: If successful, this work could point to new treatments that block inflammatory bone loss in arthritis without harming normal bone repair or the immune system.
How similar studies have gone: Previous lab and animal studies showed RBP-J can restrain TNF-driven osteoclast formation, but targeting Hs2st1 as a downstream mechanism is a new and largely untested approach in humans.
Where this research is happening
-
Hospital for Special Surgery
New York, United States Active
Researchers
- Principal investigator: Zhao, Baohong — Hospital for Special Surgery
- Study coordinator: Zhao, Baohong
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About this research
- This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
- Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
- For full project details, budget, and progress reports, visit the official NIH RePORTER page.