Anne‐Katrin Rohlfing

This study shows ACKR3 is released on extracellular vesicles under both basal and ligand-induced conditions, sequestering chemokines and opioid peptides and modulating their signaling.

This study shows hemin activates platelets and promotes thrombosis, which can be inhibited by ACKR3 agonists, suggesting a potential therapeutic strategy for atherosclerotic plaque vulnerability.

This study shows that ACKR3 agonism promotes heterodimerization with CXCR4 in platelets, reducing platelet activation and thrombus formation by modulating CXCR4 signaling.