Novel Mechanistic Risk Mapping of California Wildfire-Induced Endothelial Dysfunction-Linked Cardiac Arrhythmia

Overview

The California wildfires of 2025 (Palisades and Eaton) were the second-worst recorded weather disasters, with potential severe health consequences. It is becoming clear that cardiac abnormalities are among the emerging health concerns. My transcriptomic analysis showed that KCNH2, a gene implicated in cardiac conduction, was downregulated in the PM2.5-exposed mouse aorta and heart muscle. I then used human aortic endothelial cells to develop a novel risk-mapping model for cardiac abnormalities associated with wildfire smoke. Water samples containing wildfire smoke pollutants collected after the first rains in Eaton were co-incubated with the cells along with IL6. Results showed that Wildfire smoke-exposed cells had a significant downregulation of KCNH2 and VE-Cadherin proteins. Interestingly, wildfire smoke pollutants triggered NADPH oxidase-mediated oxidative stress, which downregulated KCNH2 and VE-Cadherin, thus establishing KCNH2 as a novel biomarker and assigning a role of NOX in the wildfire smoke-induced cardiac abnormalities, a novel finding with substantial clinical impact.

Competition history

• CSEF 2026 Medicine & Physiology (Senior Division) · Entry S-15-08

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