How fat cells drive artery inflammation in atherosclerosis
Official title: NKA/CD36 signaling in adipocytes promotes oxidative stress and drives chronic inflammation in atherosclerosis
Funded at Medical College of Wisconsin · NIH-11303332 · Data updated 2026-11-12
This project looks at how signals from fat cells can trigger artery inflammation that leads to heart attacks and strokes.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Medical College of Wisconsin NIH-funded |
| Lab location | 1 site (Milwaukee, United States) |
| Project start | April 1, 2023 |
| Project end | March 31, 2027 |
| Funding year | 2026 |
| Award (this year) | $523,513 |
| NIH project number | 5R01HL164460-04 |
| Project ID | NIH-11303332 on NIH RePORTER |
Who could benefit from this research
✓Could help
People with atherosclerotic cardiovascular disease, high cholesterol, or a history of heart attack or stroke would be most relevant to future applications of this research.
✕Less likely to help
Patients with conditions unrelated to artery plaque, such as isolated rhythm problems, or those with very advanced end-stage disease may not get direct benefit from this lab-focused work.
What this research studies
Researchers will examine how fat-cell particles called exosomes carry inflammatory signals that activate immune cells in artery walls. The team will focus on the CD36 receptor and the Na/K-ATPase protein in fat cells and macrophages to see how they create a harmful signaling loop. Work will use lab-grown cells and animal models to trace the molecular steps that increase oxidative stress and plaque formation. The goal is to identify points where new treatments could block these damaging signals.
Why it matters
Potential benefit: If successful, this work could point to new drug targets to lower artery inflammation and reduce the risk of heart attack and stroke.
How similar studies have gone: Previous animal and lab studies show blocking CD36 or lowering oxidative stress can reduce plaque inflammation, but targeting adipocyte-derived exosomes and Na/K-ATPase signaling is a newer approach.
Where this research is happening
-
Medical College of Wisconsin
Milwaukee, United States Active
Researchers
- Principal investigator: Silverstein, Roy L — Medical College of Wisconsin
- Study coordinator: Silverstein, Roy L
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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.