Why heart nerves become overactive in chronic heart failure
Official title: Mechanisms of cardiac sympathetic hyperactivity in chronic heart failure
Funded at University of Nebraska Medical Center · NIH-11237983 · Data updated 2026-11-12
This project looks at how support cells and immune cells near heart nerves may cause too much nerve activity that leads to dangerous heart rhythms in people with advanced 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 | July 1, 2017 |
| Project end | December 31, 2026 |
| Funding year | 2026 |
| Award (this year) | $632,166 |
| NIH project number | 5R01HL137832-08 |
| Project ID | NIH-11237983 on NIH RePORTER |
Who could benefit from this research
✓Could help
People with advanced heart failure, especially those whose condition followed a heart attack and who experience frequent ventricular arrhythmias, would be the group most likely to benefit from therapies developed from this work.
✕Less likely to help
Patients with mild heart failure, non-ischemic causes of heart failure, or arrhythmias driven by genetic channel problems may be less likely to benefit from approaches targeting sympathetic nerve remodeling.
What this research studies
Researchers will use laboratory models of heart attack–related heart failure to study how satellite glia (support cells) and macrophages (immune cells) interact with the nerves that control the heart. They will record nerve activity in conscious and anesthetized animals and study cells, molecules, and genes in tissue samples to see how these interactions change nerve structure and function. The team will test whether changing macrophage behavior can prevent or reverse nerve remodeling and reduce the dangerous ventricular arrhythmias that cause sudden death. Findings are intended to point toward new targets for therapies that calm overactive heart nerves.
Why it matters
Potential benefit: If successful, this work could identify new ways to reduce nerve-driven dangerous heart rhythms and lower sudden death risk in advanced heart failure.
How similar studies have gone: Previous animal and human research has linked sympathetic overactivity to arrhythmia and shown that reducing nerve activity can lower events, but the specific role of satellite glia–macrophage interactions is a newer area mostly explored in preclinical studies.
Where this research is happening
-
University of Nebraska Medical Center
Omaha, United States Active
Researchers
- Principal investigator: Li, Yu-Long — University of Nebraska Medical Center
- Study coordinator: Li, Yu-Long
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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.