Inflammation and thrombosis

Authors

  • C. T. Esmon

    1. Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation; Departments of Pathology, and Biochemistry & Molecular Biology, University of Oklahoma Health Sciences Center; and Howard Hughes Medical Institute, Oklahoma City, Oklahoma, USA
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Dr Charles T. Esmon, Oklahoma Medical Research Foundation, Cardiovascular Biology Research Program, 825 NE 13th Street, Oklahoma City, OK 73104, USA.
Tel.: +405 271 6474; fax: +405 271 3137; e-mail: Charles-Esmon@omrf.ouhsc.edu

Abstract

Summary.  Systemic inflammation is a potent prothrombotic stimulus. Inflammatory mechanisms upregulate procoagulant factors, downregulate natural anticoagulants and inhibit fibrinolytic activity. In addition to modulating plasma coagulation mechanisms, inflammatory mediators appear to increase platelet reactivity. In vivo, however, natural anticoagulants not only prevent thrombosis, but they also dampen inflammatory activity. Some insights into the evolution and linkages between inflammatory mechanisms and the coagulation/anticoagulation mechanisms have become evident from recent structural studies. This review will summarize the interactions between inflammation and coagulation.

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