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Related Concept Videos

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...
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...
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...
Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...
Peripheral Artery Disease I: Introduction01:30

Peripheral Artery Disease I: Introduction

Peripheral artery disease (PAD) predominantly results from atherosclerosis, which involves the accumulation of fatty deposits, or plaques, within the walls of arteries. This causes them to narrow and harden, significantly reducing blood flow. PAD predominantly affects the legs, particularly the arteries supplying the thighs and calves. In rare cases, it may involve other arteries, including those in the arms.Etiology of PAD:The principal cause of PAD is atherosclerosis, which results from fatty...
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...

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Related Experiment Video

Updated: Jun 9, 2026

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

Activated platelets and atherosclerosis.

Pål Aukrust1, Bente Halvorsen, Thor Ueland

  • 1Research Institute for Internal Medicine, Oslo University Hospital Rikshospitalet, N-0027 Oslo, Norway. pal.aukrust@rikshospiatlet.no

Expert Review of Cardiovascular Therapy
|September 11, 2010
PubMed
Summary
This summary is machine-generated.

Platelets are key drivers of atherosclerosis, promoting inflammation and thrombus formation. Current anti-platelet drugs are insufficient, highlighting the need for novel therapies targeting platelet inflammation.

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Ferric Chloride-induced Murine Thrombosis Models
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Last Updated: Jun 9, 2026

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

Ferric Chloride-induced Murine Thrombosis Models
10:37

Ferric Chloride-induced Murine Thrombosis Models

Published on: September 5, 2016

Area of Science:

  • Cardiovascular Biology
  • Inflammation Research
  • Hematology

Background:

  • Platelets play a critical role in atherogenesis beyond thrombus formation.
  • Emerging evidence identifies platelets as potent inflammatory cells.

Purpose of the Study:

  • To elucidate the role of platelets in inflammatory pathways driving atherosclerosis.
  • To investigate the bidirectional communication between platelets and other cells in atherosclerosis.

Main Methods:

  • Review of existing literature on platelet function in atherogenesis.
  • Analysis of cellular interactions involving platelets, leukocytes, and endothelial cells.

Main Results:

  • Platelets actively induce inflammatory responses in leukocytes and endothelial cells.
  • Platelets can also respond to inflammatory mediators from neighboring cells.
  • Platelet-mediated inflammation contributes to both early and late stages of atherosclerosis.
  • Bidirectional cell interactions involving platelets perpetuate non-resolving inflammation in atherosclerosis.

Conclusions:

  • Platelet-mediated inflammatory pathways are integral to atherogenesis.
  • Existing anti-platelet therapies do not fully address platelet-driven inflammation in atherosclerosis.
  • Novel therapeutic strategies targeting platelet inflammatory pathways are required.