Platelet-monocyte aggregates: molecular mediators of thromboinflammation
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Platelet-monocyte aggregates: molecular mediators of thromboinflammation. / Rolling, Christina C; Barrett, Tessa J; Berger, Jeffrey S.
in: FRONT CARDIOVASC MED, Jahrgang 10, 2023, S. 960398.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Review › Forschung
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TY - JOUR
T1 - Platelet-monocyte aggregates: molecular mediators of thromboinflammation
AU - Rolling, Christina C
AU - Barrett, Tessa J
AU - Berger, Jeffrey S
N1 - © 2023 Rolling, Barrett and Berger.
PY - 2023
Y1 - 2023
N2 - 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.
AB - 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.
U2 - 10.3389/fcvm.2023.960398
DO - 10.3389/fcvm.2023.960398
M3 - SCORING: Review article
C2 - 37255704
VL - 10
SP - 960398
JO - FRONT CARDIOVASC MED
JF - FRONT CARDIOVASC MED
SN - 2297-055X
ER -
