Inhibiting this pathway or knocking down endothelial NF-<i>κ</i>B effectively attenuated pro-inflammatory responses in cardiac vascular endothelial cells and reduced leukocyte infiltration after stroke.<h4>Discussion</h4>Our findings reveal a systemic mechanism for Stroke-Heart Syndrome, where ischemic stroke triggers persistent pro-inflammatory activation of cardiac vascular endothelial cells via the NF-<i>κ</i>B/NLRP3 axis. The gene discussed is NLRP3; the disease is Stroke.