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Description

Coronary artery disease (CAD) is a leading cause of death in the U.S., driven by atherosclerosis and leading to myocardial infarction (MI). Vulnerable plaque can rupture without obstructive CAD, releasing inflammatory and thrombotic proteins. Interferon signaling is implicated in this process. The hypothesis is that circulating interferon levels are associated with vulnerable plaque even without obstructive CAD. Two cohorts were analyzed: the PROMISE study (1,700 patients with chest pain, including 12% Caucasian) and the Miami Heart Study (2,352 healthy individuals, 85% Caucasian, 47% Hispanic/Latino). Inflammatory proteins were measured using the Olink platform for specificity and efficiency. Logistic regression models assessed interferon associations with CAD and vulnerable plaque. IFN-gamma levels were higher in the PROMISE cohort. IL-18, IL-18R1, and IL-12B were assessed, with IL-18 showing the strongest correlation to interferon activity. Interferon proteins are associated with CAD and vulnerable plaque, activating macrophages and promoting inflammatory protein secretion. These proteins may serve as clinically relevant biomarkers for CAD.

Publication Date

4-1-2025

Keywords

coronary artery disease, CAD, vulnerable plaque, myocardial infarction, interferon signaling, inflammatory proteins, IFN-gamma, IL-18, IL-12B, IL-18R1, PROMISE study, Miami Heart Study, biomarker discovery, macrophage activation, atherosclerosis, logistic regression, Olink platform, cardiovascular biomarkers

The Role of Interferons in Vulnerable Plaque

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