Targeting YAP and TAZ with statins to prevent transplant rejection from donor antibodies
Official title: Targeting the transcriptional co-activators YAP and TAZ with statins to prevent solid organ transplant rejection by HLA donor specific antibodies
Funded at University of California Los Angeles · NIH-11374827 · Data updated 2026-11-12
A study to see if statins can block specific gene regulators (YAP and TAZ) to protect transplanted organs from rejection caused by donor antibodies.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of California Los Angeles NIH-funded |
| Lab location | 1 site (Los Angeles, United States) |
| Project start | July 19, 2023 |
| Project end | June 30, 2028 |
| Funding year | 2026 |
| Award (this year) | $710,735 |
| NIH project number | 5R01AI173050-04 |
| Project ID | NIH-11374827 on NIH RePORTER |
Who could benefit from this research
✓Could help
Patients who have received solid organ transplants and have donor-specific antibodies may be eligible for future applications of these findings.
✕Less likely to help
Patients without donor-specific antibodies or those not undergoing transplantation may not directly benefit.
What this research studies
This project looks at how antibodies against donor tissue trigger changes in the lining of blood vessels in transplanted organs and cause damage over time. It proposes using statins to interrupt a key cellular pathway (YAP/TAZ) that drives heart and other organ transplant injury. By understanding and blocking these signals, the research aims to reduce chronic rejection and blood vessel disease after transplantation. The work would involve experiments on human cells and models to identify how blocking YAP/TAZ affects endothelial cell behavior relevant to graft survival.
Why it matters
Potential benefit: If successful, this work could lead to new strategies to prevent chronic rejection and improve long-term transplant success.
How similar studies have gone: Previous work suggests targeting related signaling pathways can influence endothelial cell behavior relevant to transplant vasculopathy, but direct YAP/TAZ targeting in this context is exploratory.
Where this research is happening
-
University of California Los Angeles
Los Angeles, United States Active
Researchers
- Principal investigator: Reed, Elaine F — University of California Los Angeles
- Study coordinator: Reed, Elaine F
Related research
Other NIH-funded projects on the same topics.
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Immunological mechanisms behind treatment-resistant kidney transplant rejection
This grant explores why certain kidney transplant rejections don’t respond to standard treatments and what immune cells in the graft are driving that resistance.
-
Understanding how BK virus links infection to kidney transplant rejection
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A multi-center study using blood biomarkers to guide how immunosuppressive drugs are given to liver transplant patients.
-
Using blood biomarkers to guide immunosuppression after liver transplant
This project uses regular blood biomarker checks to help doctors personalize immunosuppression for people who have had a liver transplant to reduce rejection and protect the kidneys.
-
Predicting acute rejection in children after heart transplant
A study to improve how doctors predict if a child who has had a heart transplant will have acute rejection using noninvasive blood markers and advanced heart MRI analysis.
-
A new biologic medicine to help prevent organ rejection
This project develops a single engineered protein designed to stop transplant rejection in people by blocking harmful immune signals and boosting protective immune cells.
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.