{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,5]],"date-time":"2026-11-05T20:41:08Z","timestamp":1793911268692,"version":"4.8.0"},"reference-count":68,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,2,19]],"date-time":"2026-02-19T00:00:00Z","timestamp":1771459200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Cardiovasc. Med."],"abstract":"<jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>Ischemic stroke elevates the risk of recurrent vascular events via endothelial cell activation-driven systemic inflammation, yet the existence and mechanisms of stroke-induced sustained pro-inflammatory changes in cardiac vascular endothelial cells remain unclear.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      The male rat distal middle cerebral artery occlusion (dMCAO) model was established. The NF-\n                      <jats:italic>\u03ba<\/jats:italic>\n                      B\/NLRP3 pathway and cardiac vascular endothelial cell activation were evaluated using proteomics analysis, immunohistochemistry, western blotting, quantitative real-time polymerase chain reaction, adeno-associated virus administration, and pharmacological interventions.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Ischemic stroke induced persistent cardiac vascular endothelial cell activation and upregulated VCAM-1\/ICAM-1, which was mediated by NF-\n                      <jats:italic>\u03ba<\/jats:italic>\n                      B\/NLRP3 signaling activation. Inhibiting this pathway or knocking down endothelial NF-\n                      <jats:italic>\u03ba<\/jats:italic>\n                      B effectively attenuated pro-inflammatory responses in cardiac vascular endothelial cells and reduced leukocyte infiltration after stroke.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Discussion<\/jats:title>\n                    <jats:p>\n                      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-\n                      <jats:italic>\u03ba<\/jats:italic>\n                      B\/NLRP3 axis. This identifies the NF-\n                      <jats:italic>\u03ba<\/jats:italic>\n                      B\/NLRP3-VCAM1\/ICAM-1 pathway as a potential therapeutic target for preventing recurrent cardiac vascular events post-ischemic stroke.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fcvm.2026.1673693","type":"journal-article","created":{"date-parts":[[2026,2,19]],"date-time":"2026-02-19T07:14:31Z","timestamp":1771485271000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":4,"title":["NF-\u03baB aggravates cardiac vascular endothelial injury by sustained activation of the NLRP3 inflammasome after ischemic stroke in rats"],"prefix":"10.3389","volume":"13","author":[{"given":"Shufeng","family":"Zhong","sequence":"first","affiliation":[{"name":"Department of Cardiology, Nanhai People\u2019s Hospital, The Sixth Affiliated Hospital of South China University of Technology","place":["Foshan, 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