Remodeling the Blood Coagulation Cascade

@article{Hoffman2004RemodelingTB,
  title={Remodeling the Blood Coagulation Cascade},
  author={M. Hoffman},
  journal={Journal of Thrombosis and Thrombolysis},
  year={2004},
  volume={16},
  pages={17-20}
}
  • M. Hoffman
  • Published 2004
  • Medicine
  • Journal of Thrombosis and Thrombolysis
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… Expand
A cell-based model of coagulation and its implications
TLDR
The cell-based model of hemostasis replaces the traditional "cascade" hypothesis, and proposes that coagulation takes place on different cell surfaces in four overlapping steps: initiation, amplification, propagation and termination. Expand
Mechanism Action of Platelets and Crucial Blood Coagulation Pathways in Hemostasis
TLDR
The aim of this review is to summarize and highlight the important pathways involved in achieving hemostasis that are ruled by platelets and describe the mechanism action of platelets, including adhesion, activation, aggregation, and coagulation, as well as the factors that aid in he mostasis and wound healing. Expand
The cell-basedmodel of coagulation
TLDR
The recently proposed model incorporates the vital role of cells in coagulation processes, and corrects deficiencies of the older cascade models, which are flawed as a description of how hemostasis occurs in vivo. Expand
Blood coagulation and its regulation by anticoagulant pathways: genetic pathogenesis of bleeding and thrombotic diseases
TLDR
The formation of the platelet plug provides the initial occlusion of the vascular lesion and is temporally co‐ordinated with the activation of the coagulation system, which occurs in response to the rupture of endothelium and the exposure of blood to the extravascular tissue. Expand
Interactions between coagulation and complement—their role in inflammation
TLDR
An appreciation of the precise relationship between complement activation and thrombosis may facilitate the development of novel therapeutics, as well as improve the clinical management of patients withThrombotic conditions that are characterized by complement-associated inflammatory responses. Expand
Hemostasis in the Lab, Approaching to the Correct Diagnosis in the Coagulopathies
Coagulation is the result of a coordinated interaction of blood proteins, circulating cells, endothelium cells and extracellular matrix proteins in the vessel wall. This process works in conjunctionExpand
The cell-based model of coagulation.
TLDR
The recently proposed model incorporates the vital role of cells in coagulation processes, and corrects deficiencies of the older cascade models, which are flawed as a description of how hemostasis occurs in vivo. Expand
The cell-based model of coagulation
TLDR
The recently proposed model incorporates the vital role of cells in coagulation processes, and corrects deficiencies of the older cascade models. Expand
An ensemble view of thrombin allostery
TLDR
Recent data are reviewed that demonstrate that apo-thrombin is zymogen-like and exists as an ensemble of conformations and how ligand binding to thrombin allosterically stabilizes conformations on the continuum from zymogene to protease is described. Expand
The inhibiting effect of factor XIII on hyperfibrinolysis.
TLDR
An in vitro model of hyperfibrinolysis could be modified by coagulation factors including factor XIII, prothrombin complex concentrate, recombinant factor VIIa, tranexamic acid, or saline as a control as measured by ROTEM is evaluated. Expand
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 20 REFERENCES
A cell-based model of hemostasis.
TLDR
This model emphasizes the importance of specific cellular receptors for the coagulation proteins and explains some aspects of hemostasis that a protein-centric model does not. Expand
AN ENZYME CASCADE IN THE BLOOD CLOTTING MECHANISM, AND ITS FUNCTION AS A BIOCHEMICAL AMPLIFIER
AFTER years of confusion, it seems that a relatively simple pattern is emerging from present theories of blood coagulation. Its recognition is assisted by the Roman numeral terminology of theExpand
An Enzyme Cascade in the Blood Clotting Mechanism, and its Function as a Biochemical Amplifier
TLDR
It has been shown that contact activates Factor XII (Hageman factor) perhaps by unfolding its molecule, which leads successively to the activation of Factors XI (PTA) and IX (Christmas factor), and X (Stuart–Prower factor), the evidence suggesting that all these reactions are enzymatic. Expand
Cellular interactions in hemostasis.
TLDR
Using a cell-based in vitro model system, it is shown that where a factor is located, not simply how much is activated, is critically important in determining its role in hemostasis. Expand
Transmission of a procoagulant signal from tissue factor‐bearing cells to platelets
  • D. Monroe, M. Hoffman, H. Roberts
  • Chemistry, Medicine
  • Blood coagulation & fibrinolysis : an international journal in haemostasis and thrombosis
  • 1996
TLDR
It is concluded that sufficient thrombin generation occurs on the TF-bearing cell (or TF- bearing vesicle) in the absence of platelets, to provide the procoagulant signal that leads to platelet activation. Expand
Factor IX is activated in vivo by the tissue factor mechanism.
TLDR
The data indicate that factor IXa generation in vivo results mainly from the activity of the tissue factor mechanism rather than the contact system (factor XII, prekallikrein, high molecular-weight kininogen, factor XI). Expand
The effect of factor X level on thrombin generation and the procoagulant effect of activated factor VII in a cell‐based model of coagulation
TLDR
It is found that only a very small amount of FX ‐ equivalent to about 3% of the normal plasma level ‐ was required to support a ‘normal’ level of thrombin generation, which suggests that, under normal conditions in vivo, the level of FX does not significantly affect hemostatic function. Expand
Hemostatic factors in rabbit limb lymph: relationship to mechanisms regulating extravascular coagulation.
TLDR
The data are compatible with a basal factor VIIa-tissue factor-catalyzed extravascular activation of factor X that is prevented from progressing to generation of fibrin in limb interstitial fluid and lymph by low levels of factor VIII and factor V and by the inhibitory activity of antithrombin and tissue factor pathway inhibitor. Expand
The effects of activated factor VII in a cell-based model for tissue factor-initiated coagulation.
  • M. Kjalke, D. Monroe, +4 authors H. Roberts
  • Chemistry, Medicine
  • Blood coagulation & fibrinolysis : an international journal in haemostasis and thrombosis
  • 1998
TLDR
Competition of active site-inhibited FVIIa with FFR-FVIIa in various cell-based assays mimicking TF-initiated coagulation illustrated the importance of activated factor VII in coagulating tissue factor initiated by tissue factor (TF). Expand
Activated protein C cleaves factor Va more efficiently on endothelium than on platelet surfaces.
TLDR
It is concluded that in vivo, despite the important role of the protein C system in regulating thrombosis, activated protein C does not serve as a primary regulator of platelet-dependent thrombin generation. Expand
...
1
2
...