Platelet-monocyte aggregates: molecular mediators of thromboinflammation.

Autor: Rolling CC; 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., Barrett TJ; Department of Medicine, New York University Grossman School of Medicine, New York, NY, United States., Berger JS; Department of Medicine, New York University Grossman School of Medicine, New York, NY, United States.
Jazyk: angličtina
Zdroj: Frontiers in cardiovascular medicine [Front Cardiovasc Med] 2023 May 15; Vol. 10, pp. 960398. Date of Electronic Publication: 2023 May 15 (Print Publication: 2023).
DOI: 10.3389/fcvm.2023.960398
Abstrakt: 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.
Competing Interests: Jeffrey Berger is PI for the NIH-funded ACTIV4a trial investigating P2Y12 inhibitors in patients hospitalized with COVID-19. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
(© 2023 Rolling, Barrett and Berger.)
Databáze: MEDLINE