Oxidative stress, mitochondria, and heart failure in a mouse model and future neonatal heart failure studies
Official title: Oxidative Stress and Mitochondrial Dysfunction in Chemogenetic Heart Failure
Funded at Brigham and Women's Hospital · NIH-11389401 · Data updated 2026-11-12
A mentored clinician–scientist program will study how oxidative stress affects heart cell powerplants and heart function, using a special mouse model, with plans to apply findings to neonatal heart disease in the future.
Quick facts
| Grant type | Career grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Brigham and Women's Hospital NIH-funded |
| Lab location | 1 site (Boston, United States) |
| Project start | August 1, 2023 |
| Project end | July 31, 2028 |
| Funding year | 2026 |
| Award (this year) | $168,220 |
| NIH project number | 5K08HL168240-04 |
| Project ID | NIH-11389401 on NIH RePORTER |
Who could benefit from this research
✓Could help
Adults or neonates with risk factors related to premature birth and oxidative stress-related heart injury; future studies may include neonatal heart failure models.
✕Less likely to help
Individuals without risk factors for oxidative stress-related cardiac injury or those not participating in any future translational steps may not benefit.
What this research studies
This five-year K08 program trains a clinician-scientist to study how reactive oxygen species damage heart metabolism and mitochondria, potentially uncovering new paths to prevent heart failure. The project uses a transgenic mouse that produces hydrogen peroxide in the heart to explore mitochondrial dysfunction and the role of Sirt3. The PI aims to translate these insights toward understanding and future study of heart failure in premature infants. The work blends mentored research with career development to support independent investigation after the award.
Why it matters
Potential benefit: If successful, this work could reveal targets to reduce oxidative damage in the heart and guide strategies to prevent or mitigate heart failure in vulnerable populations.
How similar studies have gone: Preclinical models have shown that oxidative stress can impair mitochondrial function and contribute to heart failure, supporting the approach's relevance, with this project extending to a novel chemogenetic model.
Where this research is happening
-
Brigham and Women's Hospital
Boston, United States Active
Researchers
- Principal investigator: Spyropoulos, Fotios — Brigham and Women's Hospital
- Study coordinator: Spyropoulos, Fotios
Related research
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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.