Tiny separations at heart cell connections that may cause arrhythmias
Arrhythmia Mechanisms Modulated by Intercalated Disc Extracellular Nanodomains
This project looks at whether tiny separations between heart cells make dangerous heart rhythms more likely in people with Brugada syndrome or arrhythmogenic cardiomyopathy.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Virginia Polytechnic Inst and St Univ NIH-funded |
| Lab location | 1 site (Blacksburg, United States) |
| Project ID | NIH-11293399 on NIH RePORTER |
What this research studies
The team is examining how small gaps at the connections between heart muscle cells (the intercalated disc) change electrical signals in the heart. They will use lab tissue and animal models to create swelling in the heart and test whether that swelling reveals hidden problems in sodium channels and junction proteins linked to Brugada syndrome and arrhythmogenic cardiomyopathy. The researchers will compare different experimental conditions that can mask or unmask conduction problems, with special attention to the right ventricle where these diseases often appear. Their work aims to see if managing these tiny cell separations or tissue swelling could prevent dangerous arrhythmias.
Who could benefit from this research
Good fit: People diagnosed with Brugada syndrome or arrhythmogenic cardiomyopathy, especially those with right‑ventricle involvement or known mutations affecting intercalated disc proteins, would be the most relevant candidates.
Not a fit: Patients whose arrhythmias are caused mainly by other conditions (such as coronary artery disease or structural heart problems unrelated to intercalated disc proteins) are less likely to benefit directly from this project.
Why it matters
Potential benefit: If successful, this work could point to new ways to prevent or reduce life‑threatening arrhythmias by targeting cell‑to‑cell connections or controlling heart tissue swelling.
How similar studies have performed: Previous laboratory studies have shown that electrolyte environment and gap‑junction proteins like connexin43 can hide or reveal conduction defects, but applying these findings to Brugada syndrome and arrhythmogenic cardiomyopathy in intact tissue is a newer approach.
Where this research is happening
Blacksburg, United States
- Virginia Polytechnic Inst and St Univ — Blacksburg, United States (Active)
Researchers
- Principal investigator: Poelzing, Steven — Virginia Polytechnic Inst and St Univ
- Study coordinator: Poelzing, Steven
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.