{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T15:01:39Z","timestamp":1790434899885,"version":"4.1.0"},"reference-count":70,"publisher":"American Society of Hematology","issue":"11","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2022,3,17]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Platelet ACKR3\/CXCR7 surface expression is enhanced and influences prognosis in coronary artery disease (CAD) patients, who exhibit a distinct atherothrombotic platelet lipidome. Current investigation validates the potential of ACKR3\/CXCR7 in regulating thromboinflammatory response through its impact on the platelet lipidome. CAD patients with enhanced platelet ACKR3\/CXCR7 expression exhibited reduced aggregation. Pharmacological CXCR7 agonist (VUF11207) significantly reduced prothrombotic platelet response in blood from acute coronary syndrome patients ex vivo. CXCR7 agonist administration reduced thrombotic functions and thromboinflammatory plateletleukocyte interactions post\u2013myocardial infarction and arterial injury in vivo. ACKR3\/CXCR7 ligation did not affect surface availability of surface receptors, coagulation profile, bleeding time, plasma-dependent thrombin generation (thrombinoscopy), or clot formation (thromboelastography) but counteracted activation-induced phosphatidylserine exposure and procoagulant platelet-assisted thrombin generation. Targeted (micro-UHPLC-ESI-QTrap-MS\/MS) and untargeted (UHPLCESI-QTOF-MS\/MS) lipidomics analysis revealed that ACKR3\/CXCR7 ligation favored generation of antithrombotic lipids (dihomo-\u03b3-linolenic acid [DGLA], 12-hydroxyeicosatrienoic acid [12-HETrE]) over cyclooxygenase-1 (COX-1) or 12-lipoxygenase (12-LOX) metabolized prothrombotic and phospholipase-derived atherogenic lipids in healthy subjects and CAD patients, contrary to antiplatelet therapy. Through 12-HETrE, ACKR3\/CXCR7 ligation coordinated with G\u03b1s-coupled prostacyclin receptor to trigger cyclic adenosine monophosphate\/protein kinase A\u2013mediated platelet inhibition. ACKR3\/CXCR7 ligation reduced generation of lipid agonists and lipid signaling intermediates, which affected calcium mobilization, intracellular signaling, and consequently platelet interaction with physiological matrices and thromboinflammatory secretome. This emphasized its functional dichotomy from prothrombotic CXCR4. Moreover, CXCR7 agonist regulated heparin-induced thrombocytopenia\u2013sera\/immunoglobulin G\u2013triggered platelet and neutrophil activation, heparin-induced platelet aggregation, generation of thromboinflammatory lipids, platelet-neutrophil aggregate formation, and thromboinflammatory secretion ex vivo. Therefore, ACKR3\/CXCR7 may offer a novel therapeutic strategy in acute\/chronic thromboinflammation exaggerated cardiovascular pathologies and CAD.<\/jats:p>","DOI":"10.1182\/blood.2021013097","type":"journal-article","created":{"date-parts":[[2021,12,14]],"date-time":"2021-12-14T19:56:30Z","timestamp":1639511790000},"page":"1722-1742","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":51,"title":["Platelet ACKR3\/CXCR7 favors antiplatelet lipids over an\u00a0atherothrombotic lipidome and regulates thromboinflammation"],"prefix":"10.1182","volume":"139","author":[{"given":"Malgorzata","family":"Cebo","sequence":"first","affiliation":[{"name":"Institute of Pharmaceutical Sciences, University of T\u00fcbingen, T\u00fcbingen, Germany;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kristina","family":"Dittrich","sequence":"additional","affiliation":[{"name":"Institute of Pharmaceutical Sciences, University of 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