Perinuclear RyR2 and heart cell signaling network in hypertrophy
Official title: Perinuclear Ryanodine Receptors and Cardiac Remodeling
Funded at University of Connecticut Sch of Med/dnt · NIH-11385428 · Data updated 2026-11-12
A heart researcher is exploring how specialized calcium signals near the cell nucleus control harmful heart muscle growth, with the goal of finding new therapies.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Connecticut Sch of Med/dnt NIH-funded |
| Lab location | 1 site (Farmington, United States) |
| Project start | July 1, 2023 |
| Project end | June 30, 2027 |
| Funding year | 2026 |
| Award (this year) | $545,160 |
| NIH project number | 5R01HL166547-04 |
| Project ID | NIH-11385428 on NIH RePORTER |
Who could benefit from this research
✓Could help
Patients with or at risk for pathological cardiac hypertrophy who may benefit from therapies targeting Ca2+-dependent gene expression pathways.
✕Less likely to help
Patients without cardiac hypertrophy or related signaling abnormalities may not benefit from this approach.
What this research studies
This project investigates how a specific pool of RyR2 receptors near the nucleus, in concert with mAKAPβ, creates calcium signals that drive gene programs behind pathological heart enlargement. By comparing perinuclear RyR2 function to the traditional calcium channels involved in contraction, the study aims to pinpoint distinct signaling microdomains. The work combines molecular biology, imaging, and genetic approaches to test whether disrupting this perinuclear signaling can prevent hypertrophy. The outcomes could reveal new targets for drugs that stop or reverse harmful heart remodeling without disturbing normal heart function.
Why it matters
Potential benefit: If successful, the findings could lead to therapies that prevent or reduce pathological heart enlargement by targeting perinuclear calcium signaling.
How similar studies have gone: Previous work supports a role for mAKAPβ and CaN in hypertrophy, and this project extends those findings to a perinuclear calcium signaling mechanism, which is promising but still exploratory.
Where this research is happening
-
University of Connecticut Sch of Med/dnt
Farmington, United States Active
Researchers
- Principal investigator: Dodge-Kafka, Kimberly L — University of Connecticut Sch of Med/dnt
- Study coordinator: Dodge-Kafka, Kimberly L
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.