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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...
Inflammation01:38

Inflammation

Overview
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

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.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
Introduction to Hemostasis01:05

Introduction to Hemostasis

Hemostasis is a complex physiological process that prevents excessive bleeding when a blood vessel is injured. It's crucial for maintaining the integrity of the circulatory system, as it ensures that our blood remains fluid while still within the vascular network and yet clots to prevent blood loss upon vessel injury.
The three phases of hemostasis involve many clotting factors present in plasma and several substances released by platelets and injured tissue cells. It is a fast, localized, and...
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.

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Related Experiment Video

Updated: Jul 17, 2026

An In Vitro Assay to Study Platelet Migration Using RGD-Functionalized Avidin-Biotin Tethers
05:43

An In Vitro Assay to Study Platelet Migration Using RGD-Functionalized Avidin-Biotin Tethers

Published on: November 8, 2024

Platelets as mediators of inflammation.

Steven R Steinhubl1

  • 1Division of Cardiology, University of Kentucky, 900 South Limestone Avenue, 326 Charles T. Wellington Building, Lexington, KY 40536-0200, USA. steinhubl@uky.edu

Hematology/Oncology Clinics of North America
|January 30, 2007
PubMed
Summary

Inflammation drives atherosclerosis progression. Platelets, once seen as passive responders, are now known key inflammatory mediators, influencing disease development and treatment response.

Area of Science:

  • Cardiovascular Biology
  • Inflammation Research
  • Hematology

Background:

  • Atherosclerosis is a chronic inflammatory disease.
  • Platelets play a crucial role in inflammation beyond hemostasis.
  • Inflammatory mediators released by platelets contribute to atherosclerotic plaque development.

Purpose of the Study:

  • To review the evolving understanding of platelet involvement in atherosclerosis.
  • To explore the link between platelet activation and inflammatory processes.
  • To examine the relationship between inflammation markers and antiplatelet therapy efficacy.

Main Methods:

  • Literature review of current research on inflammation and atherosclerosis.
  • Analysis of studies investigating platelet activation and mediator release.

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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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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

Microfluidics in Assessing Platelet Function
06:47

Microfluidics in Assessing Platelet Function

Published on: November 8, 2024

Related Experiment Videos

Last Updated: Jul 17, 2026

An In Vitro Assay to Study Platelet Migration Using RGD-Functionalized Avidin-Biotin Tethers
05:43

An In Vitro Assay to Study Platelet Migration Using RGD-Functionalized Avidin-Biotin Tethers

Published on: November 8, 2024

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

Microfluidics in Assessing Platelet Function
06:47

Microfluidics in Assessing Platelet Function

Published on: November 8, 2024

  • Examination of data correlating inflammatory markers with clinical outcomes of antiplatelet treatment.
  • Main Results:

    • Platelets are active participants in the inflammatory cascade of atherosclerosis.
    • Platelet activation releases numerous proinflammatory proteins.
    • Preliminary data suggest inflammation markers may predict antiplatelet therapy benefits.

    Conclusions:

    • Platelets are central players in atherosclerosis pathogenesis through inflammatory mechanisms.
    • Further research is needed to clarify the predictive role of inflammation markers for antiplatelet therapy.
    • Understanding platelet-driven inflammation may offer new therapeutic targets for atherosclerosis.