How COVID-19 causes blood clots and tiny microclots
Mechanisms of Thrombosis in SARS CoV-2 Infection
['FUNDING_R01'] · UNIVERSITY OF KENTUCKY · NIH-11258033
This work looks at why people with COVID-19 develop blood clots and tiny microclots that may lead to lasting tissue damage.
Quick facts
| Phase | ['FUNDING_R01'] |
|---|---|
| Study type | Nih_funding |
| Sex | All |
| Sponsor | UNIVERSITY OF KENTUCKY (nih funded) |
| Locations | 1 site (LEXINGTON, UNITED STATES) |
| Trial ID | NIH-11258033 on ClinicalTrials.gov |
What this research studies
Researchers will collect blood and other samples from people during acute COVID-19 illness and from people with lingering (long COVID) symptoms, and they will study those samples in the laboratory alongside cell and animal models. From early work they identified two ways clots may form: blood vessel cells release von Willebrand Factor (VWF) that traps a protective protein called protein S, and high levels of lipids and an inhibitor called PAI-1 block the clot-dissolving protein tPA. The team will measure these proteins, image microclots, and test how changing these pathways affects clot formation and breakdown. Their goal is to learn whether these combined problems create stable microclots that could explain localized tissue damage and persistent symptoms.
Who could benefit from this research
Good fit: Ideal candidates would include people with recent COVID-19 infection, hospitalized patients with clotting signs, and people experiencing long COVID symptoms who can provide blood samples.
Not a fit: People without a history of COVID-19 or whose health issues are unrelated to clotting are unlikely to benefit directly from this work.
Why it matters
Potential benefit: If successful, this could point to new treatments to prevent or dissolve microclots and lower the risk of long-term complications after COVID-19.
How similar studies have performed: Prior studies have shown COVID-19 raises clotting risk and that thrombotic events matter for outcomes, but the specific VWF–protein S interaction and the dyslipidemia/PAI-1 effect on tPA are relatively new mechanisms being explored.
Where this research is happening
LEXINGTON, UNITED STATES
- UNIVERSITY OF KENTUCKY — LEXINGTON, UNITED STATES (ACTIVE)
Researchers
- Principal investigator: WOOD, JEREMY P — UNIVERSITY OF KENTUCKY
- Study coordinator: WOOD, JEREMY P
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 below.