Stellate Gland Nrf2 Signaling and Heart–Nerve Interactions 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-11402729 · Data updated 2026-11-12
A study in people is not required; instead, this grant focuses on how the brain and nerves control heart problems in chronic heart failure through a key protective pathway called Nrf2.
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 | 2026 |
| Award (this year) | $726,683 |
| NIH project number | 5R01HL172029-03 |
| Project ID | NIH-11402729 on NIH RePORTER |
Who could benefit from this research
✓Could help
Ideal candidates are individuals with chronic heart failure or a history of myocardial infarction who may one day benefit from therapies targeting neural pathways or oxidative-stress regulation.
✕Less likely to help
Patients without heart failure or those not involved in neural-related mechanisms may not directly benefit from this research.
What this research studies
This project investigates how oxidative stress and nerve signaling in the stellate ganglia contribute to worse heart failure. By studying changes in Nrf2 signaling and related inflammatory and redox pathways after heart injury, researchers aim to understand how these processes drive harmful sympathetic activity to the heart. The work includes measuring molecules and proteins in neural tissues and testing how altering Nrf2 affects neural inflammation and oxidative stress in animal models. The findings could point to new approaches to reduce arrhythmias and improve heart function by stabilizing nerve signals to the heart.
Why it matters
Potential benefit: If successful, the work could lead to new strategies to limit damaging nerve activity to the heart and reduce arrhythmias in heart failure patients.
How similar studies have gone: Previous studies show that modifying Nrf2 can alter sympathetic signaling and oxidative stress in animal models, supporting the potential for benefit in humans.
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.