Activation of HIF2 in Cardiac Vasculature Leads to Arterial Remodeling, Dilation, Thrombosis, and Inflammation, Recapitulating Cardiac Involvement in Kawasaki Disease
Authors' conclusion
Our findings establish HIF2 as a central driver of coronary inflammation, vascular remodeling, and thrombotic complications resembling those observed in severe KD.
Study context
- Population
- Mice with genetic hyperactivation of the hypoxia pathway in coronary vessel and cardiac fibroblast progenitors; cardiac tissue from patients with fatal Kawasaki disease (KD) coronary aneurysms
- Comparison
- Vhl conditional knockout vs Vhl/Hif2a double deletion
- Outcome
- Cardiovascular phenotype of Vhl conditional knockout (Wt1 lineage) mice and Hif2a rescue
Methodological detailsmouse model, human tissue immunohistochemistry
- Mouse model
- Human tissue immunohistochemistry
Main finding
As reported in the abstract
Sudden death, likely due to vessel rupture (age, weeks)
15–20
Original publication
Activation of HIF2 in Cardiac Vasculature Leads to Arterial Remodeling, Dilation, Thrombosis, and Inflammation, Recapitulating Cardiac Involvement in Kawasaki Disease. Circulation. Published 8 June 2026. doi:10.
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