NF-κB aggravates cardiac vascular endothelial injury by sustained activation of the NLRP3 inflammasome after ischemic stroke in rats

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. This identifies the NF-<i>κ</i>B/NLRP3-VCAM1/ICAM-1 pathway as a potential therapeutic target for preventing recurrent cardiac vascular events post-ischemic stroke.