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Updated: Jul 15, 2026

Ferric Chloride-induced Murine Thrombosis Models
Published on: September 5, 2016
Chemokines and thrombogenicity
Michele P Lambert1, Bruce S Sachais, M Anna Kowalska
1Division of Hematology, Children's Hospital of Philadelphia, 3615 Civic Center Blvd ARC Rm. 316I, Philadelphia, PA 19104, USA.
Thrombosis is an important clinical entity, and pathologic thrombosis, in the form of atherosclerosis, is a major cause of morbidity and mortality. Recent research points to the role of chemokines, normally key factors in inflammation, in thrombogenesis. Many recent studies in murine transgenic and knockout models show that chemokines and their receptors are important modulators of the process of thrombus formation, particularly in atherosclerosis. Platelet-released chemokines can potentiate or inhibit thrombosis and inflammation. This review focuses on the role of chemokines in platelet activation and thrombosis, particularly as it relates to atherosclerosis. Further studies to define this complex interaction are underway.
Thrombosis is an important clinical entity, and pathologic thrombosis, in the form of atherosclerosis, is a major cause of morbidity and mortality. Recent research points to the role of chemokines, normally key factors in inflammation, in thrombogenesis. Many recent studies in murine transgenic and knockout models show that chemokines and their receptors are important modulators of the process of thrombus formation, particularly in atherosclerosis. Platelet-released chemokines can potentiate or inhibit thrombosis and inflammation. This review focuses on the role of chemokines in platelet activation and thrombosis, particularly as it relates to atherosclerosis. Further studies to define this complex interaction are underway.
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