Blood Coagulation Signaling Pathways

Click on the appropriate button below to highlight the factors involved in either the extrinsic or intrinsic pathway of blood coagulation or the common factors required for both pathways. Then click on the fibrinolysis button to see the process by which a fibrin clot is broken down.

Activated
Platelets
Activated
Platelets
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GPVI
GPVI
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GPIb-V-IX
GPIb-V-IX
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vWF
vWF
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Collagen IV
Collagen IV
RBC
RBC
WBC
WBC
Activated
Platelets
Activated
Platelets
Blood clot
Blood clot

Wound Healing

Wound Healing

Basement Membrane
Basement Membrane
Coag. Factor X
Coag. Factor X
Coag. Factor Xa
Coag. Factor Xa
Ca2+
Ca2+
Coag. Factor Xa
Coag. Factor Xa
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Coag. Factor Va
Coag. Factor Va
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Membrane
Phospholipid
Membrane
Phospholipid
Coag. Factor II/
Prothrombin
Coag. Factor II/
Prothrombin
Coag. Factor IIa/
Thrombin
Coag. Factor IIa/
Thrombin
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Coag. Factor V
Coag. Factor V
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Coag. Factor Va
Coag. Factor Va
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Fibrinogen
Fibrinogen
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Fibrin
Fibrin
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Coag. Factor XIII
Coag. Factor XIII
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Coag. Factor XIIIa
Coag. Factor XIIIa
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Thrombomodulin
Thrombomodulin
Coag. Factor XIV/
Protein C
Coag. Factor XIV/
Protein C
Coag. Factor XIVa/
Activated Protein C
Coag. Factor XIVa/
Activated Protein C
Coag. Factor XIVa/
Activated Protein C
Coag. Factor XIVa/
Activated Protein C
Protein S
Protein S
Coag. Factor VIII
Coag. Factor VIII
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Coag. Factor VIIIa
Coag. Factor VIIIa
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Coag. Factor Va
Coag. Factor Va
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Serpin A5
Serpin C1
Serpin D1
Serpin A5
Serpin C1
Serpin D1
Serpin A5
Serpin A5
Positive Feedback
Loop
Positive Feedback
Loop
Negative
Feedback
Negative
Feedback
Negative
Feedback
Negative
Feedback
Fibrin clot
Fibrin clot
Ca2+
Ca2+
Ca2+
Ca2+
Coag. Factor III/TF
Coag. Factor III/TF
Coag. Factor VII
Coag. Factor VII
Coag. Factor VIIa
Coag. Factor VIIa
Membrane
Phospholipid
Membrane
Phospholipid
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TFPI
TFPI
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Ca2+
Ca2+
Positive Feedback
Loop
Positive Feedback
Loop
Positive Feedback
Loop
Positive Feedback
Loop
Serpin E1
Serpin B2
Serpin A5
Serpin E1
Serpin B2
Serpin A5
Plasminogen
Plasminogen
uPA or tPA
uPA or tPA
Plasmin
Plasmin
Serpin F2
alpha2-Macroglobulin
Serpin F2
alpha2-Macroglobulin
Fibrin clot
Fibrin clot

Fibrinolysis

Fibrinolysis

HMW Kininogen
HMW Kininogen
Prekallikrein
Prekallikrein
Negatively Charged Surface
Negatively Charged Surface
Coag. Factor XII
Coag. Factor XII
Coag. Factor XIIa
Coag. Factor XIIa
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Plasma Kallikrein
Plasma Kallikrein
Coag. Factor XI
Coag. Factor XI
Coag. Factor XIa
Coag. Factor XIa
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Coag. Factor IX
Coag. Factor IX
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Coag. Factor IXa
Coag. Factor IXa
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Coag. Factor IXa
Coag. Factor IXa
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Coag. Factor VIIIa
Coag. Factor VIIIa
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Membrane
Phospholipid
Membrane
Phospholipid
Ca2+
Ca2+
Ca2+
Ca2+
Ca2+
Ca2+
Vessel Lumen
Vessel Lumen

Blood Vessel Damage

Blood Vessel Damage

Overview of the Extrinsic and Intrinsic Pathways of Blood Coagulation

Injuries that damage blood vessels promote blood coagulation to initiate hemostasis and prevent excessive blood loss. Blood coagulation results from a series of proteolytic reactions involving the step-wise activation of coagulation factors. Subsets of these factors can be activated by two distinct pathways, the extrinsic or tissue damage pathway, and the intrinsic or contact pathway. The extrinsic pathway of coagulation is initiated as a result of contact between the bloodstream and Coagulation Factor III/Tissue Factor, a glycoprotein constitutively expressed on the surface of subendothelial tissues that is exposed upon vascular injury. Coagulation Factor III/TF forms a complex with Coagulation Factor VIIa and phospholipid that activates Coagulation Factor Xa in the presence of Ca2+. Coagulation Factor Xa acts with Coagulation Factor Va to cleave Prothrombin/Coagulation Factor II, which subsequently cleaves Fibrinogen to produce Fibrin. The slower, intrinsic pathway of coagulation provides an alternate mechanism for activation of Coagulation Factor Xa. It is initiated when Coagulation Factor XII, Prekallikrein, and high molecular weight Kininogen are exposed to a negatively charged surface. This results in cleavage and activation of Coagulation Factor XIIa, which activates Coagulation Factor XIa. Coagulation Factor XIa subsequently cleaves and activates Coagulation Factor IXa. Coagulation Factor IXa forms a complex with Coagulation Factor VIIIa and phospholipid that then activates Coagulation Factor Xa. Events downstream of the activation of Coagulation Factor Xa are common to both the intrinsic and extrinsic pathways of blood coagulation. Activated Coagulation Factor Xa cleaves Prothrombin/Coagulation Factor II to generate active Thrombin/Coagulation Factor IIa, which then cleaves Fibrinogen to produce Fibrin monomers. These monomers are cross-linked by Coagulation Factor XIIIa to from a Fibrin clot. The Fibrin clot is dissolved by Plasmin once the tissue is repaired.

In addition to directly generating active Fibrin and Coagulation Factor XIIIa, Thrombin/Coagulation Factor IIa activates Coagulation Factors V, VIII, and Protein C. These factors enhance or inhibit Thrombin production through positive or negative feedback regulation. Coagulation factors Va and VIIIa promote Thrombin production by positively regulating either the cleavage of Prothrombin itself or the cleavage and activation of Coagulation Factor Xa, respectively. In contrast, activation of Protein C by Thrombin binding to Thrombomodulin leads to the degradation of Coagulation Factors Va and VIIIa and inhibits the cleavage of Prothrombin. These forms of feedback regulation, along with sequential activation of clotting factors, allow precise control of the blood coagulation cascade. This tight regulation is critical to prevent excessive blood loss associated with too little clotting, or too much clotting, which could result in blockage of a blood vessel and lead to a heart attack or stroke.

To learn more, please visit our Coagulation Research Area.

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