Oxidative changes and aortic aneurysms in Marfan syndrome
Official title: Thiol redox signaling in aortic aneurysm
Funded at Boston University Medical Campus · NIH-11328829 · Data updated 2026-11-12
This work looks at whether reversing a chemical modification that turns off the enzyme Sirt1 in aortic wall cells can help prevent dangerous aortic enlargement in people with Marfan syndrome.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Boston University Medical Campus NIH-funded |
| Lab location | 1 site (Boston, United States) |
| Project start | May 15, 2025 |
| Project end | February 28, 2029 |
| Funding year | 2026 |
| Award (this year) | $782,413 |
| NIH project number | 5R01HL175424-02 |
| Project ID | NIH-11328829 on NIH RePORTER |
Who could benefit from this research
✓Could help
People diagnosed with Marfan syndrome (FBN1 mutation) who have or are at risk for thoracic aortic aneurysm would be the most relevant candidates for related future therapies or tissue donation.
✕Less likely to help
People whose aneurysms are caused by unrelated conditions or who already need urgent surgical repair are unlikely to benefit directly from this molecular work.
What this research studies
From a patient's viewpoint, researchers compare aortic tissue from people with Marfan syndrome and a mouse model to find chemical changes that inactivate Sirt1 in the aorta. They will study how glutathionylation (an oxidative modification) affects vascular smooth muscle cells and promotes aneurysm formation. The team plans to use molecular tools, including gene delivery methods, to restore Sirt1 activity in vessel cells and watch whether that slows or prevents aortic wall degeneration. Results will guide whether targeting this redox pathway could become a therapy to protect the aorta.
Why it matters
Potential benefit: If successful, this could lead to new treatments that slow or prevent aortic enlargement and lower the risk of dissection in people with Marfan syndrome.
How similar studies have gone: Previous work has shown increased oxidative stress in aneurysms and protective roles for Sirt1, but directly targeting Sirt1 glutathionylation as a therapy is a newer, less-tested approach.
Where this research is happening
-
Boston University Medical Campus
Boston, United States Active
Researchers
- Principal investigator: Seta, Francesca — Boston University Medical Campus
- Study coordinator: Seta, Francesca
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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.