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. 2019 Jun 3;140(4):319–335. doi: 10.1161/CIRCULATIONAHA.118.039345

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© 2019 The Authors.

Circulation is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited.

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Figure 7. — Annexin A1 (AnxA1) mitigates thromboinflammatory responses and promotes resolution during ischemia reperfusion injury.Schematic overview shows the effects of AnxA1 on both thrombotic and inflammatory events as follows. Step 1 reduces platelet–neutrophil aggregate (PNA) adhesion on endothelial cells in the cerebral microvasculature; steps 2 and 3 decrease neutrophil (step 2) and platelet adhesion (step 3); step 4 diminishes platelet activation and aggregate velocity, promoting a phosphatidylserine and P-selectin–dependent clearance program; step 5 promotes neutrophil phagocytosis of platelets for resolution; and step 6 protects against enhanced intravascular thrombus formation and secondary thrombotic events in the cerebral microvasculature. ALX indicates the lipoxin A4 receptor; and Fpr2, formyl peptide receptor 2.