Jeffrey Rade
University of Massachusetts Chan Medical School, MA·Medicine & Clinical Research
Heart failure, a condition in which the heart cannot pump enough blood to meet the body's needs, is a growing public health problem. This project asks whether thromboxane A2 (TXA2), a fat-derived signaling molecule made from arachidonic acid, helps cause heart failure.
- Fields
Medicine & Clinical Research
Public Health & Epidemiology
Genetics
- Topics
heart failure
thromboxane A2
urinary thromboxane B2 metabolites
- Grants
- 1 known grant, through Mar 2030
What they work on
- Determine whether urinary TXB2-MGFR, a kidney-corrected urine marker of thromboxane production, predicts hospitalization, death and disease severity in 3,252 heart failure patients from the EMPEROR trials, and how its 12-week change tracks treatment response.
- Relate urinary TXB2-MGFR to early heart failure risk traits in over 13,000 FHS and MESA participants, including subclinical heart damage, vessel dysfunction, exercise intolerance, platelet and immune activation, dietary fatty acids and visceral obesity.
- Identify gene variants linked to high TXB2-MGFR in more than 8,000 aspirin non-users and use them in Mendelian randomization across UK Biobank, All of Us and HERMES to test whether thromboxane causes heart failure.
- Build a thromboxane genetic risk score and test its links to heart failure risk factors and heart imaging traits using phenome-wide association studies in genetic consortia and Vanderbilt BioVU.
More about the research
TXA2 has long been linked to platelets, the blood cells that form clots, but evidence suggests it is also made in other tissues. Aspirin blocks TXA2 production in platelets but not in other cells. Higher levels of thromboxane breakdown products in urine are tied to death risk in both aspirin users and non-users. In animal models, TXA2 signaling drives scarring (fibrosis) and thickening of heart muscle.
Why it matters
Measuring urinary thromboxane could help doctors identify people at higher risk of developing heart failure, or of being hospitalized or dying from it. If excess thromboxane, made largely outside platelets, proves to drive the disease, the TXA2 pathway may become a treatment target. That would matter because aspirin does not block this non-platelet source. The work could also show which patients are most likely to benefit from therapies that act on this pathway.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
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The school
University of Massachusetts Chan Medical School: 29 labs on PI Pages, $350M a year on research, 55 research doctorates a year.
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