Targeting ACKR3/CXCR7 Enhances Platelet Anticoagulant Lipids and Modulates Procoagulant Function: Implications for Thrombosis Management

Activation of the atypical chemokine receptor CXCR7 (ACKR3) modulates platelet lipid processing, favoring anticoagulant long-chain acylcarnitines (LC-CAR) over prothrombotic lipids.
CXCR7 agonist VUF11207 preserves mitochondrial integrity and reduces platelet oxidative stress, thereby limiting procoagulant platelet activation.
The CXCR7-AMPK-ACC signaling axis promotes platelet lipolysis, reduces phosphatidylserine exposure, and diminishes FX/FXa binding, cumulatively reducing thrombin generation and thrombosis in vivo.
Targeting CXCR7 in thrombosis models decreases inflammation and procoagulant lipid mediators, highlighting its therapeutic potential in cardiovascular conditions such as STEMI and venous thromboembolism (VTE).

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

Activation of the atypical chemokine receptor CXCR7 (ACKR3) modulates platelet lipid processing, favoring anticoagulant long-chain acylcarnitines (LC-CAR) over prothrombotic lipids.
CXCR7 agonist VUF11207 preserves mitochondrial integrity and reduces platelet oxidative stress, thereby limiting procoagulant platelet activation.
The CXCR7-AMPK-ACC signaling axis promotes platelet lipolysis, reduces phosphatidylserine exposure, and diminishes FX/FXa binding, cumulatively reducing thrombin generation and thrombosis in vivo.
Targeting CXCR7 in thrombosis models decreases inflammation and procoagulant lipid mediators, highlighting its therapeutic potential in cardiovascular conditions such as STEMI and venous thromboembolism (VTE).

Sign in free to continue reading