How the CCL2/CCR2 immune signal affects artery disease and finding natural blockers
Official title: Signaling mediators of CCL2/CCR2 and natural product discovery
Funded at Charles R. Drew University of Med & Sci · NIH-11326708 · Data updated 2026-11-12
This project looks at how the CCL2/CCR2 immune signal contributes to atherosclerosis and searches for natural compounds that might block harmful inflammation for people with artery disease.
Quick facts
| Grant type | NIH-funded research |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Charles R. Drew University of Med & Sci NIH-funded |
| Lab location | 1 site (Los Angeles, United States) |
| Project start | May 1, 2023 |
| Project end | April 30, 2028 |
| Funding year | 2026 |
| Award (this year) | $361,250 |
| NIH project number | 5R35GM149318-04 |
| Project ID | NIH-11326708 on NIH RePORTER |
Who could benefit from this research
✓Could help
Adults with diagnosed atherosclerotic cardiovascular disease or people at high risk for artery plaque due to inflammation would be the most likely candidates for future trials informed by this research.
✕Less likely to help
People without artery disease, those needing immediate emergency care, or patients whose conditions are unrelated to inflammatory artery disease are unlikely to see direct benefit from this basic lab research now.
What this research studies
From a patient perspective, researchers will study how the CCL2/CCR2 signaling system works inside the cells that contribute to artery plaque using lab-grown human cells and disease models. They will map the internal cell signals triggered by CCL2/CCR2 and identify other chemokine pathways that step in when this one is blocked. The team will screen natural products to find compounds that can block harmful signaling and will test promising candidates in preclinical models. Findings could guide future clinical testing of new anti-inflammatory approaches for people with atherosclerosis.
Why it matters
Potential benefit: If successful, this work could point to new anti-inflammatory treatments or natural compound leads that reduce artery inflammation and slow or prevent atherosclerosis.
How similar studies have gone: Blocking CCL2/CCR2 showed benefit in many animal and lab models but past clinical trials of direct blockers had limited success, so this project focuses on understanding compensatory pathways and seeking alternative compounds.
Where this research is happening
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Charles R. Drew University of Med & Sci
Los Angeles, United States Active
Researchers
- Principal investigator: Wang, Piwen — Charles R. Drew University of Med & Sci
- Study coordinator: Wang, Piwen
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.