Remodeling the blood coagulation cascade.


Journal Article (Review)

The concept of a coagulation cascade describes the biochemical interactions of the coagulation factors, but has flaws as a model of the hemostatic process in vivo. For example, the model cannot explain why hemophiliacs bleed when they have an intact factor VIIa/tissue factor ("extrinsic") pathway. Hemostasis requires the formation of an impermeable platelet and fibrin plug at the site of vessel injury, but it also requires that the powerful procoagulant substances activated in this process remain localized to the site of injury. This control of blood coagulation is accomplished by localizing the procoagulant reactions to events on specific cell surfaces to keep coagulation from spreading throughout the vascular system. A consideration of the critical role of cells allows us to construct a model of coagulation that better explains bleeding and thrombosis in vivo. This cell-based model suggests that the "intrinsic" and "extrinsic" pathways are in fact not redundant systems, but operate in parallel on different cell surfaces.

Full Text

Duke Authors

Cited Authors

  • Hoffman, M

Published Date

  • August 2003

Published In

Volume / Issue

  • 16 / 1-2

Start / End Page

  • 17 - 20

PubMed ID

  • 14760207

Pubmed Central ID

  • 14760207

International Standard Serial Number (ISSN)

  • 0929-5305

Digital Object Identifier (DOI)

  • 10.1023/B:THRO.0000014588.95061.28


  • eng

Conference Location

  • Netherlands