Nrf2 signaling in the heart's sympathetic nerves in chronic heart failure
Official title: Stellate Ganglia Nrf2 Signaling and Enhanced Cardiac Sympathetic Tone in Chronic Heart Failure
Funded at University of Nebraska Medical Center · NIH-11180508 · Data updated 2026-11-12
Testing whether boosting the antioxidant regulator Nrf2 in the nerves that control the heart can calm overactive nerve signals and reduce dangerous heart rhythms in chronic heart failure.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Nebraska Medical Center NIH-funded |
| Lab location | 1 site (Omaha, United States) |
| Project start | September 1, 2024 |
| Project end | August 31, 2028 |
| Funding year | 2025 |
| Award (this year) | $741,512 |
| NIH project number | 5R01HL172029-02 |
| Project ID | NIH-11180508 on NIH RePORTER |
Who could benefit from this research
✓Could help
People with chronic heart failure following a heart attack, especially those with signs of high sympathetic activity or recurrent arrhythmias, would be most relevant to this research.
✕Less likely to help
People whose heart failure is due to non-ischemic causes or whose arrhythmias are unrelated to sympathetic nerve overactivity may not directly benefit from these nerve-focused findings.
What this research studies
This project focuses on the small nerve cluster (stellate ganglia) that sends stress signals to the heart after a heart attack and during chronic heart failure. Researchers will track inflammation, oxidative stress, and the Nrf2 antioxidant regulator over time in that nerve tissue using animal models of post-heart attack heart failure. They will raise or lower Nrf2 in those nerves and measure nerve activity, tissue oxidative damage, and heart rhythm changes to see if boosting Nrf2 calms the nerves. The work aims to point toward ways to prevent nerve-driven dangerous heart rhythms in people with heart failure.
Why it matters
Potential benefit: If successful, this could point to new treatments that reduce nerve-driven arrhythmias and lower complications after heart attack-related heart failure.
How similar studies have gone: Prior animal studies from these investigators showed that lowering Nrf2 increases nerve activity and raising Nrf2 reduces sympathetic activity and oxidative stress, but applying this approach to prevent post-MI arrhythmias is relatively new.
Where this research is happening
-
University of Nebraska Medical Center
Omaha, United States Active
Researchers
- Principal investigator: Wang, Hanjun — University of Nebraska Medical Center
- Study coordinator: Wang, Hanjun
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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.