Mitchell Dyer
Medical College of Wisconsin, WI·Medicine & Clinical Research·Early-career
A blood clot that forms in a deep leg vein, called deep venous thrombosis (DVT), is a leading cause of illness and death. Standard blood thinners such as heparins and direct oral anticoagulants (DOACs) help, yet DVT remains common in high-risk groups such as trauma patients and people with chronic inflammatory diseases, and these drugs raise bleeding risk.
- Fields
Medicine & Clinical Research
Physiology
Pharmacology
- Topics
deep venous thrombosis
post-thrombotic syndrome
fibrinogen
- Grants
- 1 known grant, through Dec 2029
What they work on
- Test whether fibrinogen controls the entry of inflammatory cells into a developing clot in post-traumatic and acute DVT, by lowering circulating fibrinogen with siRNA-loaded lipid nanoparticles in rodent and swine thrombosis models.
- Determine how fibrinogen shapes the activity of matrix metalloproteases, tissue-remodeling enzymes, during clot resolution and vein wall remodeling and fibrosis in chronic venous thrombosis.
- Use liver-targeting lipid nanoparticles carrying anti-fibrinogen siRNA to reduce fibrinogen selectively, and gather preclinical evidence on clot outcomes and on whether bleeding risk stays unchanged.
More about the research
Between 40 and 70 percent of patients later develop post-thrombotic syndrome, a lasting condition of leg pain, swelling and skin ulcers that follows a very large clot or a clot that clears poorly and leaves the vein wall scarred. Few treatments exist for it. Clot formation and clot clearance both depend on an interplay between the clotting system and inflammation.
Why it matters
Trauma patients and people with chronic inflammatory disease still develop dangerous leg clots despite current blood thinners, and those drugs carry bleeding risk. Many survivors go on to live with post-thrombotic syndrome, for which little can be offered. Clarifying how fibrinogen links clotting to inflammation and vein-wall healing could identify an RNA-based way to lower clot risk without added bleeding, and may suggest ways to prevent chronic clots and vein scarring.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Rafal Pawlinski
University of North Carolina at Chapel Hill, NC·Medicine & Clinical Research
Identify the disease-specific triggers that activate Factor XII, a protein that starts blood clotting, in sickle cell disease, using blood samples from patients and a mouse model of the disease.
Julie Jaffray
University of California-San Diego, CA·Medicine & Clinical Research·Early-career
Prospectively validate a pediatric hospital-acquired venous thromboembolism (VTE) risk assessment model from the CHAT Consortium, using a case-control design and electronic medical record review.
Yamin Li
Upstate Medical University, NY·Pharmacology
Expand the chemical diversity of sulfonium lipids — carriers that use a charged sulfur group instead of the usual amine — by adding new head, linker and tail building blocks, and relate these structures to self-assembly, mRNA delivery and biocompatibility.
The school
Medical College of Wisconsin: 17 labs on PI Pages, $360M a year on research, 44 research doctorates a year.
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