Recent clinical reports indicate that wildfire-linked particulate matter (PM) 2.5 exposures can lead to cardiac arrhythmias primarily from endothelial dysfunction. There are no established mechanistic models that study the cardiac arrhythmia risk and identify early clinical biomarkers of cardiac injury following wildfire exposure. The aim is to develop an in vitro model that identifies the molecular mediators and the mechanisms of wildfire-linked cardiac injury in PM 2.5 exposure. Firstly, I used transcriptomic analysis to identify unique molecular signatures following a long-term PM 2.5 exposure typically found in wildfire smoke. Results analyzed via a PCA plot showed a distinct separation of clusters of genes in the exposed group when compared to controls. Secondly, I used a systems biology approach for establishing causality via a connector analysis. Results showed that SOCS-3, IL6, and KCNH2, a unique protein known for its role in cardioprotection related to preventing arrhythmias, were differentially expressed, with KCNH2 downregulated in mice. The results suggested that my unique simulation of wildfire smoke exposure can downregulate KCNH2 primarily through NOX2. My study can lead to the use of KCNH2 as a unique early diagnostic marker for cardiac risk factors in wildfire exposure. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.
Chatterjee et al. (Fri,) studied this question.
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