ORIGINAL RESEARCH article
Front. Cardiovasc. Med.
Sec. General Cardiovascular Medicine
NF-κB Aggravates Cardiac Vascular Endothelial Injury by Sustained Activation of the NLRP3 Inflammasome After Ischemic Stroke in Rats
Zhong Shufeng
Xiao Yuan
Liu Junqiang
Nanhai People's Hospital, Foshan, China
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Abstract
Ischemic stroke leads to a persistently high risk of recurrent vascular events, which is caused by systemic inflammation driven by endothelial cell activation. However, whether and how ischemic stroke induces sustained pro-inflammatory endothelial alterations in cardiac vessels remains poorly understood. We showed that ischemic stroke induces persistent activation of cardiac vascular endothelial cells, as well as upregulation of the adhesion molecules VCAM1 and ICAM-1. This abnormal endothelial activity is caused by persistent activation of the NF-κB/NLRP3 signaling pathway. Furthermore, we reduced the inflammatory process in cardiac vascular endothelial cells after ischemic stroke by using NF-κB or NLRP3 inhibitors and performing knockdown of endothelial NF-κB. These findings reveal a systemic mechanism underlying the Stroke-Heart Syndrome, whereby ischemic stroke induces persistent activation of cardiac vascular endothelial cells, providing a potential therapeutic target for intervention or prevention of recurrent cardiac vascular events after ischemic stroke.
Summary
Keywords
endothelial cell, Inflammation, ischemic stroke, NF-κB signaling pathway, NLRP3 infammasome
Received
26 July 2025
Accepted
03 February 2026
Copyright
© 2026 Shufeng, Yuan and Junqiang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Liu Junqiang
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