Platelet-monocyte aggregates: molecular mediators of thromboinflammation

Frontiers in Cardiovascular Medicine

Cardiovascular Medicine

Jeffrey S. Berger¹  Tessa J. Barrett¹  Christina C. Rolling² 

[1] Department of Medicine, New York University Grossman School of Medicine, New York, NY, United States;Department of Medicine, New York University Grossman School of Medicine, New York, NY, United States;Department of Oncology and Hematology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany;

关键词: monocyte-platelet aggregates;    thromboinflammation;    antiplatelet therapy;    P2Y12 inhibitor;    inflammatory diseases;    atherosclerosis;   

DOI  :  10.3389/fcvm.2023.960398

 received in 2022-06-02, accepted in 2023-04-24,  发布年份 2023

来源: Frontiers

【 摘 要 】

Platelets, key facilitators of primary hemostasis and thrombosis, have emerged as crucial cellular mediators of innate immunity and inflammation. Exemplified by their ability to alter the phenotype and function of monocytes, activated platelets bind to circulating monocytes to form monocyte-platelet aggregates (MPA). The platelet-monocyte axis has emerged as a key mechanism connecting thrombosis and inflammation. MPA are elevated across the spectrum of inflammatory and autoimmune disorders, including cardiovascular disease, systemic lupus erythematosus (SLE), and COVID-19, and are positively associated with disease severity. These clinical disorders are all characterized by an increased risk of thromboembolic complications. Intriguingly, monocytes in contact with platelets become proinflammatory and procoagulant, highlighting that this interaction is a central element of thromboinflammation.

【 授权许可】

Unknown   
© 2023 Rolling, Barrett and Berger.