How the body‑clock gene Bmal1 controls cholesterol handling in immune cells
Official title: Bmal1, a master regulator of Macrophage cholesterol metabolism
Funded at New York University D/b/a NYU Long Island School of Medicine · NIH-11309637 · Data updated 2026-11-12
The team is working to understand how the body clock gene Bmal1 changes how immune cells handle cholesterol, which could matter for people at risk for artery plaque and heart disease.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | New York University D/b/a NYU Long Island School of Medicine NIH-funded |
| Lab location | 1 site (Mineola, United States) |
| Project start | April 1, 2024 |
| Project end | March 31, 2028 |
| Funding year | 2026 |
| Award (this year) | $523,152 |
| NIH project number | 5R01HL169313-03 |
| Project ID | NIH-11309637 on NIH RePORTER |
Who could benefit from this research
✓Could help
Ideal candidates for any future human-facing parts would be adults with atherosclerotic cardiovascular disease or high cholesterol who can donate blood or tissue samples for research.
✕Less likely to help
People without cardiovascular disease or those seeking immediate treatment are unlikely to get direct benefit from this preclinical, mouse‑focused research.
What this research studies
The researchers will use several mouse models and isolated immune cells to see how turning off Bmal1 in macrophages changes cholesterol uptake, export, and movement out of lysosomes. They will focus on molecular steps including CD36 (for uptake), ABCG1 and the repressor ZNF202 (for cholesterol efflux), and NPC1/NPC2 (for lysosomal egress), and how Bmal1 partners with NPAS2 and REV‑ERBα. Experiments combine genetic mouse models, cellular assays, and biochemical measurements to track cholesterol traffic in macrophages. The goal is to link circadian control in immune cells to plaque formation in arteries.
Why it matters
Potential benefit: If successful, this work could point to new ways to prevent or reduce atherosclerosis by correcting macrophage cholesterol handling tied to the circadian clock.
How similar studies have gone: Prior studies showed that global loss of Bmal1 worsens atherosclerosis and earlier reports on macrophage‑specific effects conflicted, but this group’s mouse experiments found macrophage Bmal1 loss increases plaque across multiple models.
Where this research is happening
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New York University D/b/a NYU Long Island School of Medicine
Mineola, United States Active
Researchers
- Principal investigator: Pan, Xiaoyue — New York University D/b/a NYU Long Island School of Medicine
- Study coordinator: Pan, Xiaoyue
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.