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Clinical data suggest that the \u03b1\n                    <jats:sub>2<\/jats:sub>\n                    \u2010adrenergic receptor (AdR\u2010\u03b1\n                    <jats:sub>2<\/jats:sub>\n                    ) agonist dexmedetomidine (Dex) can influence coagulation in stress\u2010exposed intensive care unit patients. Given the important role of protease\u2010activated receptor\u20102 (PAR\u20102) in vascular pathobiology, we aimed to investigate the potential effects of Dex on stress\u2010related thrombus formation, focusing on the PAR\u20102 signaling pathway. Eight\u2010week\u2010old male mice underwent non\u2010stress and immobilization stress with Dex treatment for 2\u2009weeks and were then subjected to carotid artery thrombosis induction using ferric chloride (FeCl\n                    <jats:sub>3<\/jats:sub>\n                    ). On Day 14 post\u2010stress, the mice exhibited increased thrombus weight and length, along with harmful alterations in the plasma levels of von Willebrand factor and metalloproteinase with thrombospondin Type 13 motifs. Additionally, arterial protein and\/or mRNA levels of PAR\u20102, p\u2010Akt, Bcl\u20102, cleaved caspase\u20103, cytochrome\n                    <jats:italic>c<\/jats:italic>\n                    , gp91\n                    <jats:sup>phox<\/jats:sup>\n                    , TNF\u2010\u03b1, MCP\u20101, ICAM\u20101, VCAM\u20101, and TLR\u20104 were altered, accompanied by arterial endothelial loss. Dex treatment reversed these changes. Conversely, AdR\u2010\u03b12 blockage with yohimbine diminished the benefits of Dex. In\u00a0vitro, Dex reduced stress serum\u2010induced reactive oxygen species production and endothelial apoptosis, along with beneficial alterations in PAR\u20102, Bcl\u20102, and cytochrome\n                    <jats:italic>c<\/jats:italic>\n                    protein levels. Yohimbine diminished these effects. Thus, \u03b1\n                    <jats:sub>2<\/jats:sub>\n                    \u2010adrenergic receptor activation appeared to mitigate stress\u2010related thrombus formation in mice undergoing FeCl\n                    <jats:sub>3<\/jats:sub>\n                    \u2010induced surgery, possibly by negatively regulating PAR\u20102 signaling. These findings suggest a potential therapeutic strategy for CPS\u2010related thrombotic events in patients with TCVDs.\n                  <\/jats:p>","DOI":"10.1096\/fj.202500724r","type":"journal-article","created":{"date-parts":[[2025,4,30]],"date-time":"2025-04-30T23:09:47Z","timestamp":1746054587000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Dexmedetomidine Reduces Chronic Stress\u2013Related Thrombosis in a Mouse\n                    <scp>\n                      FeCl\n                      <sub>3<\/sub>\n                    <\/scp>\n                    Model"],"prefix":"10.1096","volume":"39","author":[{"given":"Huazhen","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Anesthesiology Yanbian University Hospital  Yanji Jilin P.R. 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