Epigenetic clues to stop heart scarring and failure
Official title: Epigenomic mechanisms of cardiac fibrosis and heart failure
Funded at J. David Gladstone Institutes · NIH-11415521 · Data updated 2026-11-12
A patient-focused look at how turning off specific epigenetic signals may reduce heart scarring and improve heart function in people with heart failure.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | J. David Gladstone Institutes NIH-funded |
| Lab location | 1 site (San Francisco, United States) |
| Project start | September 12, 2025 |
| Project end | May 31, 2029 |
| Funding year | 2026 |
| Award (this year) | $773,842 |
| NIH project number | 5R01HL175312-02 |
| Project ID | NIH-11415521 on NIH RePORTER |
Who could benefit from this research
✓Could help
Adults with heart failure or at risk of heart failure who have signs of myocardial fibrosis.
✕Less likely to help
People without heart failure or those without myocardial fibrosis may not directly benefit from this research.
What this research studies
This project studies how the DNA packaging system in heart cells drives scarring and worsening heart failure, using insights from human data and mouse models to identify targets that could be blocked by drugs. Researchers have found that BET proteins help turn on genes that promote fibrosis, and stopping BET activity may curb this process. The study builds on single-cell analyses to pinpoint key genes like MEOX1 that become active during disease and tests how blocking these pathways affects heart tissue in models that resemble human disease. If successful, these efforts could lead to therapies that more precisely prevent fibrosis without harming other tissues.
Why it matters
Potential benefit: If the approach works, patients with heart failure could experience less scar tissue in the heart and better heart function.
How similar studies have gone: Earlier studies in animals and human cells suggest BET inhibition can reduce cardiac fibrosis and dysfunction, supporting potential clinical relevance.
Where this research is happening
-
J. David Gladstone Institutes
San Francisco, United States Active
Researchers
- Principal investigator: Alexanian, Michael — J. David Gladstone Institutes
- Study coordinator: Alexanian, Michael
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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.