Key result
EPAS1 attenuates atherosclerosis initiation at disturbed flow sites by promoting endothelial fatty acid uptake.
Atherosclerotic plaques form unevenly due to disturbed blood flow, causing localized endothelial cell (EC) dysfunction. Obesity exacerbates this process, but the underlying molecular mechanisms are unclear. The transcription factor EPAS1 (HIF2A) has regulatory roles in endothelium, but its involvement in atherosclerosis remains unexplored. This study investigates the potential interplay between EPAS1, obesity, and atherosclerosis.
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Pirri et al. (2024) studied Atherosclerosis. EPAS1 was evaluated. EPAS1 attenuates atherosclerosis initiation at disturbed flow sites through endothelial fatty acid uptake.
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