How mechanical stress interacts with MYBPC3 gene changes in hypertrophic cardiomyopathy
Official title: Biomaterial Platforms to Model the Role of Mechanical Overload in MYBPC3-Linked Hypertrophic Cardiomyopathy
Funded at Washington University · NIH-11166519 · Data updated 2026-11-12
Looks at whether extra mechanical stress on the heart makes people with MYBPC3 gene changes develop or keep hypertrophic cardiomyopathy, using tiny lab-grown human heart tissues.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Washington University NIH-funded |
| Lab location | 1 site (Saint Louis, United States) |
| Project start | September 1, 2021 |
| Project end | August 31, 2026 |
| Funding year | 2025 |
| Award (this year) | $393,750 |
| NIH project number | 5R01HL159094-05 |
| Project ID | NIH-11166519 on NIH RePORTER |
Who could benefit from this research
✓Could help
People who carry MYBPC3 gene mutations or have hypertrophic cardiomyopathy linked to MYBPC3 would be most relevant to this work.
✕Less likely to help
People whose heart thickening is caused by other genes or non-genetic factors, or those needing urgent clinical treatment, are unlikely to get direct benefit from this lab-based research.
What this research studies
This project uses small human 'micro-heart' tissues grown from induced pluripotent stem cells that carry MYBPC3 gene changes to mimic patient hearts. Researchers apply controlled levels of stretch and pressure to these tissues and measure changes in structure, contractile function, and gene activity over time. They compare tissues with and without MYBPC3 mutations to see whether mutations change how much stress causes lasting thickening and whether lowering stress can reverse it. The goal is to connect mechanical load with the molecular signals that drive hypertrophic remodeling in MYBPC3-linked HCM.
Why it matters
Potential benefit: Could help explain why some people with MYBPC3 mutations develop HCM and guide better ways to prevent or reverse harmful heart thickening.
How similar studies have gone: Clinical and animal studies suggest mechanical stress affects hypertrophy, but using human stem-cell micro-heart models to map these effects is relatively new.
Where this research is happening
-
Washington University
Saint Louis, United States Active
Researchers
- Principal investigator: Huebsch, Nathaniel — Washington University
- Study coordinator: Huebsch, Nathaniel
Related research
Other NIH-funded projects on the same topics.
-
SGLT inhibitors for non-obstructive hypertrophic cardiomyopathy
A testing of a diabetes drug class (SGLT2 inhibitors) to help people with non-obstructive hypertrophic cardiomyopathy feel better and reduce heart-related problems.
-
Using big biobanks to understand rare gene changes in hypertrophic cardiomyopathy
A large study will look at genetic data and health information from many people to better understand how rare gene changes influence hypertrophic cardiomyopathy and its risks.
-
Understanding heart disease in hypertrophic cardiomyopathy through heart tissue and blood analysis
Researchers are studying people with hypertrophic cardiomyopathy to see how genes and signaling in heart tissue and blood relate to disease progression and risk of serious heart problems.
-
Myosin binding protein C variants and heart disease
A doctor-scientist at the University of Michigan is studying how certain genetic changes in a heart protein (MYBPC3) cause hypertrophic cardiomyopathy and whether fixing the protein or its interactions could help people with this condition.
-
MEK inhibitor for severe infantile heart failure in Noonan and related RASopathies
A 12-month, multi-site trial tests whether the medicine trametinib can help infants with life-threatening heart failure due to Noonan syndrome and related genetic conditions.
-
MEK inhibitor shows promise for serious infant heart disease in Noonan/RASopathies
A multi-site study tests whether the drug trametinib can help infants with severe heart muscle thickening caused by Noonan syndrome and related RASopathies.
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.