Patients surviving a stroke are at increased risk for subsequent cardiovascular events and accelerated atherosclerosis. Roth and colleagues now show that stroke exacerbates atherosclerosis progression via alarmin-mediated propagation of vascular inflammation. Recruitment of activated monocytes via the CC-chemokine ligand 2–CC-chemokine receptor type 2 pathway was critical in stroke-induced vascular inflammation. Neutralization of circulating alarmins or knockdown of the receptor for advanced glycation end products (RAGE), attenuated atheroprogression. The findings identify a synergistic effect of the sympathetic stress response and alarmin-driven inflammation via RAGE as a critical mechanism of exacerbated atherosclerosis progression after stroke.
Roth S, Singh V, Tiedt S, Schindler L, Huber G, Geerlof A, Antoine DJ, Anfray A, Orset C, et al: Brain-released alarmins and stress response synergize in accelerating atherosclerosis progression after stroke. Science Translational Medicine 10(432): eaao1313 (2018);
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