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Related Concept Videos

Formation of the Platelet Plug01:22

Formation of the Platelet Plug

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The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
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Extrinsic and Intrinsic Pathways of Hemostasis01:20

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Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which...
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Structure and Function of Platelets01:18

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The cell fragments known as platelets are disc-shaped, with an average diameter of about 3 μm and a thickness of roughly 1 μm. They play a crucial role in the body's vascular clotting system, which also involves plasma proteins, blood cells, and blood vessel tissues.
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Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
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Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

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After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
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Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

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Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
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Related Experiment Video

Updated: Mar 20, 2026

Helical Organization of Blood Coagulation Factor VIII on Lipid Nanotubes
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Novel aspects of platelet factor XIII function.

Joanne L Mitchell1, Nicola J Mutch1

  • 1Institute of Medical Sciences, University of Aberdeen, Aberdeen, UK.

Thrombosis Research
|May 22, 2016
PubMed
Summary

Platelet factor XIII-A (FXIII-A) has novel intracellular and extracellular roles in hemostasis. This review explores recent findings on these functions, expanding our understanding of blood clotting mechanisms.

Keywords:
factor XIIIfibrinfibrinolysisplateletsα(2)-antiplasmin

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Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
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Related Experiment Videos

Last Updated: Mar 20, 2026

Helical Organization of Blood Coagulation Factor VIII on Lipid Nanotubes
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A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time
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A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time

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Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
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Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation

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Area of Science:

  • Hematology
  • Biochemistry
  • Molecular Biology

Background:

  • Factor XIII (FXIII) is present in plasma and hematopoietic cells, including platelets.
  • The cellular form, FXIII-A, was traditionally considered to function solely intracellularly due to the absence of a signal sequence.
  • Emerging evidence indicates significant roles for platelet FXIII-A beyond intracellular functions.

Purpose of the Study:

  • To review recent advances in understanding the functions of platelet factor XIII-A (FXIII-A).
  • To discuss both novel intracellular and extracellular roles of platelet FXIII-A in hemostasis.
  • To highlight the expanding knowledge of FXIII-A's contribution to blood clotting.

Main Methods:

  • This work is a condensed review of existing literature.
  • It synthesizes recent findings on platelet FXIII-A.
  • Focuses on both intracellular and extracellular mechanisms.

Main Results:

  • Platelet FXIII-A exhibits diverse mechanisms modulating hemostasis.
  • Evidence supports both intracellular and extracellular functions.
  • These functions contribute significantly to overall hemostatic processes.

Conclusions:

  • Platelet FXIII-A plays critical roles in hemostasis through both intracellular and extracellular activities.
  • Further research is warranted to fully elucidate these complex functions.
  • Understanding these roles enhances knowledge of blood coagulation and potential therapeutic targets.