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Submitted on June 16, 2005
Accepted on October 19, 2005
From the Pathology and Laboratory Medicine Service (M.H.), Durham Veterans Affairs Medical Center and Department of Pathology, Duke University Medical Center, Durham, and Carolina Cardiovascular Biology Center and Department of Medicine (D.M.M., M.H.), University of North Carolina, Chapel Hill, NC.
* To whom correspondence should be addressed. E-mail: maureane.hoffman{at}med.va.gov.
Abstract--The coagulation process has been conceptualized as being primarily dependent on adequate levels of the coagulation proteins. This concept was based on the clear relationship between the bleeding tendency and factor levels in hemophilia. The field is now evolving toward conceptualizing coagulation as being actively regulated by the specialized cellular components of the process. Rather than conceiving coagulation as only a "cascade" of proteolytic reactions, the coagulation reactions occur as overlapping steps on cell surfaces. Components of the old "extrinsic" and "intrinsic" pathways of coagulation can be thought of as participating in the initiation and propagation of coagulation reactions, respectively. Thus, these pathways are not redundant as they are portrayed in the cascade model, but play distinct and complementary roles. Our understanding of how specific cellular features control the processes of hemostasis and thrombosis is developing rapidly. This review discusses some aspects of the cellular control of coagulation.
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