Why heart nerves become overactive in chronic heart failure
Mechanisms of cardiac sympathetic hyperactivity in chronic heart failure
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 ID | NIH-11237983 on NIH RePORTER |
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.
Who could benefit from this research
Good fit: 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.
Not a fit: 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.
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 performed: 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
Omaha, United States
- 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
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 below.