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Related Concept Videos

Formation of the Platelet Plug01:22

Formation of the Platelet Plug

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...
Structure and Function of Platelets01:18

Structure and Function of Platelets

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.
Platelets are continually replenished, circulating in the bloodstream for 9-12 days before being removed by phagocytes, primarily in the spleen. A microliter of circulating blood contains between 150,000 and 450,000 platelets, with...
Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

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...
Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

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.
Disorders of Hemostasis01:24

Disorders of Hemostasis

Hemostasis, the process that stops bleeding after a blood vessel injury, is crucial for maintaining the integrity of the circulatory system. However, disorders of hemostasis can disrupt this delicate balance, leading to either excessive clotting or bleeding. These disorders can be broadly classified into thromboembolic disorders and bleeding disorders.
Thromboembolic Disorders
Two factors primarily cause thromboembolic conditions.
Atherosclerosis I: Introduction01:30

Atherosclerosis I: Introduction

Atherosclerosis is a progressive disorder characterized by the buildup of plaques on the arterial inner wall, causing them to narrow and harden over time. These plaques comprise lipids, calcium, blood components, carbohydrates, and fibrous tissue. The process primarily affects the intima of large and medium-sized arteries, reducing blood flow in any artery.Etiology and risk factorsThe cause of atherosclerosis is multifactorial, involving a complex interplay among endothelial injury, lipid...

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Related Experiment Video

Updated: May 19, 2026

Ferric Chloride-induced Murine Thrombosis Models
10:37

Ferric Chloride-induced Murine Thrombosis Models

Published on: September 5, 2016

Platelets in atherosclerosis and thrombosis.

Christian Schulz1, Steffen Massberg

  • 1Deutsches Herzzentrum and I. Medizinische Klinik, Klinikum rechts der Isar, Technische Universitaet Muenchen, Munich, Germany. chrisschulz@mytum.de

Handbook of Experimental Pharmacology
|August 25, 2012
PubMed
Summary

Platelets are crucial in arterial thrombosis and atherosclerosis. Understanding platelet receptor roles and interactions with immune cells offers new therapeutic targets for vascular diseases.

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Real-time Imaging of Heterotypic Platelet-neutrophil Interactions on the Activated Endothelium During Vascular Inflammation and Thrombus Formation in Live Mice
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Last Updated: May 19, 2026

Ferric Chloride-induced Murine Thrombosis Models
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Ferric Chloride-induced Murine Thrombosis Models

Published on: September 5, 2016

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
04:37

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

Published on: May 23, 2025

Real-time Imaging of Heterotypic Platelet-neutrophil Interactions on the Activated Endothelium During Vascular Inflammation and Thrombus Formation in Live Mice
11:18

Real-time Imaging of Heterotypic Platelet-neutrophil Interactions on the Activated Endothelium During Vascular Inflammation and Thrombus Formation in Live Mice

Published on: April 2, 2013

Area of Science:

  • Cardiovascular Biology
  • Hematology
  • Immunology

Background:

  • Atherosclerotic plaque rupture initiates arterial thrombus formation.
  • Platelets are key players in both acute thrombosis and chronic atherogenesis.

Purpose of the Study:

  • To delineate the sequence of events in arterial thrombus formation.
  • To dissect the specific roles of platelet receptors in thrombosis.
  • To describe platelet involvement in atherosclerotic lesion development.

Main Methods:

  • Analysis of platelet tethering and activation.
  • Investigation of platelet-immune cell interactions.
  • Examination of platelet-secreted molecules in inflammation.

Main Results:

  • Platelet activation is triggered by thrombogenic matrix exposure.
  • Extracellular nucleosomes mediate fibrin formation via immune cell interplay.
  • Platelets promote leukocyte recruitment and inflammation in the arterial wall.

Conclusions:

  • Platelets are central to arterial thrombosis and atheroprogression.
  • Targeting platelet function presents a promising therapeutic strategy for vascular diseases.