How epigenetics guide the heart as it forms before birth
Official title: Epigenetic regulation in cardiac development
Funded at Texas A&m University Health Science Ctr · NIH-11333051 · Data updated 2026-11-12
This project looks at how TET proteins that change DNA markings help the heart form in embryos and whether a mother's metabolism affects that process.
Quick facts
| Grant type | NIH-funded research |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Texas A&m University Health Science Ctr NIH-funded |
| Lab location | 1 site (College Station, United States) |
| Project start | April 1, 2023 |
| Project end | March 31, 2030 |
| Funding year | 2026 |
| Award (this year) | $935,316 |
| NIH project number | 5R35HL166557-04 |
| Project ID | NIH-11333051 on NIH RePORTER |
Who could benefit from this research
✓Could help
People who are pregnant or planning pregnancy, especially those with metabolic conditions (for example diabetes or obesity) or families with a history of congenital heart defects, would be most relevant to this line of research.
✕Less likely to help
Adults with heart conditions caused by acquired disease later in life (unrelated to fetal heart development) are unlikely to receive direct benefit from these findings in the near term.
What this research studies
Researchers study how TET family enzymes control the timing and location of gene activity needed for normal heart formation using molecular and genetic experiments. They use mouse models with cardiac-specific TET deletion to see how changes in chromatin structure and enhancer-promoter interactions disrupt heart development. The team also examines abnormal gene programs linked to lipid metabolism in TET-deficient hearts and tests whether prenatal maternal metabolic stressors alter TET-related pathways. Findings combine tissue-level analysis, genomics, and developmental biology to connect molecular mechanisms to congenital heart abnormalities.
Why it matters
Potential benefit: If successful, this work could clarify causes of some congenital heart defects and point to prevention or early-intervention strategies related to maternal health.
How similar studies have gone: Previous mouse studies have shown TET proteins are essential for heart development and can cause noncompaction cardiomyopathy when deleted, and this project builds on those established preclinical results while exploring new links to maternal metabolism.
Where this research is happening
-
Texas A&m University Health Science Ctr
College Station, United States Active
Researchers
- Principal investigator: Huang, Yun — Texas A&m University Health Science Ctr
- Study coordinator: Huang, Yun
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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.