Hemostasis is a physiologic mechanism that maintains blood ina fluid state within the circulation. The coagulation of bloodis mediated by cellular components and soluble plasma proteins.In response to vascular injury, circulating platelets adhere,aggregate, and provide cell-surface phospholipid for the assemblyof blood-clotting enzyme complexes. The extrinsic pathway ofblood coagulation is initiated when blood is exposed to non-vascular-cell–boundtissue factor in the subendothelial space (Figure 1). Tissuefactor binds to activated factor VII, and the resulting enzymecomplex activates factors IX and X of the intrinsic and commoncoagulation pathways, respectively. Factor IX activated . . . [Full Text of this Article]
The Systemic-Defect–Local-Phenotype Paradox
Hypercoagulability in Humans
Animal Models of Hypercoagulability
Vascular-Bed–Specific Signaling Pathways
Extracellular Signals
Cell-Subtype–Specific Signaling Pathways
Transcriptional Regulation
Coronary-Artery Thrombosis
Conclusions
Source Information
From the Department of Medicine, Divisions of Molecular Medicine and Hematology–Oncology, Beth Israel Deaconess Medical Center, Boston (R.D.R., W.C.A.); and the Department of Biology, Massachusetts Institute of Technology, Cambridge (R.D.R.).
Address reprint requests to Dr. Aird at the Division of Molecular Medicine, RW-663, Beth Israel Deaconess Medical Center, Boston, MA 02215, or at waird@caregroup.harvard.edu.
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