RECK protein's role in harmful heart remodeling and heart failure
RECK in Adverse Cardiac Remodeling and Heart Failure
They are looking at whether boosting a protein called RECK can stop or reverse harmful heart changes that lead to heart failure in older people with pressure-related problems like high blood pressure or aortic valve narrowing.
Quick facts
| Grant type | NIH-funded research |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Harry S. Truman Memorial VA Hospital NIH-funded |
| Lab location | 1 site (Columbia, United States) |
| Project ID | NIH-11130960 on NIH RePORTER |
What this research studies
This research looks at how the protein RECK controls enzymes and signals that break down heart tissue and cause scarring after pressure-related stress such as high blood pressure or aortic valve narrowing. In the lab they will use cells and animal models, expose hearts to angiotensin II or mechanical pressure, and test whether increasing RECK (including with viral delivery tools) reduces MMP activity, limits fibroblast migration, and lowers fibrosis and muscle thickening. They will measure heart structure and function, enzyme activity, and cellular behavior to see if RECK restores healthier tissue remodeling. Although mostly preclinical, the work is intended to guide future treatments for older adults with severe left ventricular hypertrophy or heart failure.
Who could benefit from this research
Good fit: Ideal candidates would be older adults (especially 65+) with left ventricular hypertrophy or pressure-overload conditions such as aortic stenosis or long-standing hypertension, including Veterans receiving care in affiliated centers.
Not a fit: People without pressure-related heart remodeling (for example, those with purely ischemic cardiomyopathy or no signs of left ventricular hypertrophy) or much younger patients are less likely to benefit directly from this work.
Why it matters
Potential benefit: If successful, this could lead to new therapies that slow or reverse harmful heart remodeling, reduce hospitalizations, and improve outcomes for people with heart failure related to pressure overload.
How similar studies have performed: Related laboratory studies have shown that boosting RECK or blocking matrix metalloproteinases can reverse remodeling in cells and animal models, but therapies targeting RECK in people are novel and untested in clinical trials.
Where this research is happening
Columbia, United States
- Harry S. Truman Memorial VA Hospital — Columbia, United States (Active)
Researchers
- Principal investigator: Bysani, Chandrasekar — Harry S. Truman Memorial VA Hospital
- Study coordinator: Bysani, Chandrasekar
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.