Protecting heart cell energy to slow atrial fibrillation
Genes and Metabolism: Targeting Mitochondrial Dysfunction in Atrial Fibrillation
['FUNDING_P01'] · CLEVELAND CLINIC LERNER COM-CWRU · NIH-11166611
Seeing whether treatments that strengthen mitochondria (the cell's powerhouses) in atrial heart cells can reduce the electrical instability that leads to atrial fibrillation for people at risk.
Quick facts
| Phase | ['FUNDING_P01'] |
|---|---|
| Study type | Nih_funding |
| Sex | All |
| Sponsor | CLEVELAND CLINIC LERNER COM-CWRU (nih funded) |
| Locations | 1 site (CLEVELAND, UNITED STATES) |
| Trial ID | NIH-11166611 on ClinicalTrials.gov |
What this research studies
This project focuses on mitochondria—the tiny energy factories inside atrial heart cells—and how metabolic stresses like aging, obesity, alcohol, or other health problems make them produce damaging oxidants. Researchers will grow atrial-like human heart tissue from induced pluripotent stem cells and expose those tissues to metabolic stress to track mitochondrial DNA damage, gene changes, and abnormal electrical activity. They will then try interventions designed to boost mitochondrial resilience and reduce metabolic differences between cells to see if electrical irregularities are lessened. The work aims to identify treatments that could later be tested in people to slow or reverse progression of atrial fibrillation.
Who could benefit from this research
Good fit: People with atrial fibrillation or those at high risk due to factors like obesity, hypertension, sleep apnea, heavy alcohol use, or aging would be the most relevant candidates for future clinical testing.
Not a fit: Patients whose atrial fibrillation is driven primarily by large structural heart defects or unrelated genetic channelopathies may be less likely to benefit from mitochondria-focused treatments.
Why it matters
Potential benefit: If successful, this could lead to new treatments that slow or reverse AF progression and reduce complications like stroke.
How similar studies have performed: Laboratory studies have linked mitochondrial dysfunction to atrial fibrillation, but therapies that restore mitochondrial function in human AF remain largely unproven and are still being developed.
Where this research is happening
CLEVELAND, UNITED STATES
- CLEVELAND CLINIC LERNER COM-CWRU — CLEVELAND, UNITED STATES (ACTIVE)
Researchers
- Principal investigator: VAN WAGONER, DAVID R — CLEVELAND CLINIC LERNER COM-CWRU
- Study coordinator: VAN WAGONER, DAVID R
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.