Thrombospondin-4's role in protecting heart muscle cells from stress
Thrombospondin 4 regulates adaptive ER stress responseRenewal - Resubmission - 1
['FUNDING_R01'] · CINCINNATI CHILDRENS HOSP MED CTR · NIH-11242019
Looks at whether a protein called thrombospondin-4 helps heart muscle cells handle internal stress to protect people with cardiomyopathy.
Quick facts
| Phase | ['FUNDING_R01'] |
|---|---|
| Study type | Nih_funding |
| Sex | All |
| Sponsor | CINCINNATI CHILDRENS HOSP MED CTR (nih funded) |
| Locations | 1 site (CINCINNATI, UNITED STATES) |
| Trial ID | NIH-11242019 on ClinicalTrials.gov |
What this research studies
From a patient's perspective, researchers are studying proteins called thrombospondins that sit inside heart muscle cells and help manage cellular stress and membrane stability. They use genetic mouse models and cell experiments to compare what happens when different thrombospondin genes are turned on or off, and they study how these changes affect attachments (integrins) and the cell's protein-handling (ER stress) systems. The team is connecting these basic experiments to forms of heart muscle disease caused by weakened membrane anchoring, with the goal of identifying targets that could be turned into therapies. Some parts of the work are preclinical, but findings could guide future patient-focused trials or biomarker studies.
Who could benefit from this research
Good fit: People with genetic muscular dystrophies that affect the heart or those with cardiomyopathy thought to involve membrane anchoring defects would be most relevant for this line of research.
Not a fit: People with heart disease caused by unrelated factors (for example, ischemic heart disease) or those needing immediate treatment are unlikely to benefit directly from this early-stage research.
Why it matters
Potential benefit: If successful, this work could point to new ways to strengthen heart muscle cell membranes and slow or prevent cardiomyopathy in people with membrane-related heart disease.
How similar studies have performed: Prior preclinical studies showed Thbs3 can weaken membrane stability while Thbs4 can protect it, so this project builds on promising animal and cell biology findings though human therapies remain unproven.
Where this research is happening
CINCINNATI, UNITED STATES
- CINCINNATI CHILDRENS HOSP MED CTR — CINCINNATI, UNITED STATES (ACTIVE)
Researchers
- Principal investigator: MOLKENTIN, JEFFERY D — CINCINNATI CHILDRENS HOSP MED CTR
- Study coordinator: MOLKENTIN, JEFFERY D
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.
Conditions: Cardiac Diseases, Cardiac Disorders