Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

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...
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...
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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Follicular lymphoma transformed to classic Hodgkin lymphoma.

Blood·2026
Same author

Fibrin-Associated Large B-Cell Lymphoma.

International journal of laboratory hematology·2026
Same author

Hemophagocytic lymphohistiocytosis is characterized by tissue factor-driven coagulopathy, endothelial injury, and immunothrombosis.

Leukemia & lymphoma·2025
Same author

Glycoprotein VI is a receptor for the PF4/anti-PF4 IgG complex and contributes to platelet activation in heparin-induced thrombocytopenia (HIT).

Journal of thrombosis and haemostasis : JTH·2025
Same author

Soluble P-selectin, but not circulating cell-free DNA, is a potential diagnostic biomarker in heparin-induced thrombocytopenia.

Journal of thrombosis and haemostasis : JTH·2025
Same author

Idiopathic multicentric Castleman disease - TAFRO results in high levels of mTOR activator SVEP1, tissue factor, and endotheliopathy.

Blood vessels, thrombosis & hemostasis·2025

Related Experiment Video

Updated: Jun 17, 2026

A Simple Protocol for Platelet-mediated Clumping of Plasmodium falciparum-infected Erythrocytes in a Resource Poor Setting
07:27

A Simple Protocol for Platelet-mediated Clumping of Plasmodium falciparum-infected Erythrocytes in a Resource Poor Setting

Published on: May 16, 2013

Platelet aggregation inhibitors from hematophagous animals.

Ivo M B Francischetti1

  • 1Vector Biology Section, Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892-8132, USA. ifrancischetti@niaid.nih.gov

Toxicon : Official Journal of the International Society on Toxinology
|December 29, 2009
PubMed
Summary

Blood-feeding animals

Area of Science:

  • Biochemistry
  • Pharmacology
  • Molecular Biology

Background:

  • Salivary glands of blood-sucking animals secrete bioactive molecules.
  • These molecules counteract hemostasis through redundant and synergistic mechanisms.
  • Understanding these molecules is crucial for biochemical and therapeutic applications.

Purpose of the Study:

  • To review recent advances in identifying salivary inhibitors of platelet aggregation.
  • To discuss their molecular characterization and mechanisms of action.
  • To highlight the diversity and therapeutic potential of these sialogenins.

Main Methods:

  • Literature review of studies on salivary inhibitors of platelet aggregation.
  • Analysis of molecular characterization and mechanisms of action.

More Related Videos

Platelet Adhesion and Aggregation Under Flow using Microfluidic Flow Cells
10:10

Platelet Adhesion and Aggregation Under Flow using Microfluidic Flow Cells

Published on: October 27, 2009

Turbidimetry on Human Washed Platelets: The Effect of the Pannexin1-inhibitor Brilliant Blue FCF on Collagen-induced Aggregation
09:13

Turbidimetry on Human Washed Platelets: The Effect of the Pannexin1-inhibitor Brilliant Blue FCF on Collagen-induced Aggregation

Published on: April 6, 2017

Related Experiment Videos

Last Updated: Jun 17, 2026

A Simple Protocol for Platelet-mediated Clumping of Plasmodium falciparum-infected Erythrocytes in a Resource Poor Setting
07:27

A Simple Protocol for Platelet-mediated Clumping of Plasmodium falciparum-infected Erythrocytes in a Resource Poor Setting

Published on: May 16, 2013

Platelet Adhesion and Aggregation Under Flow using Microfluidic Flow Cells
10:10

Platelet Adhesion and Aggregation Under Flow using Microfluidic Flow Cells

Published on: October 27, 2009

Turbidimetry on Human Washed Platelets: The Effect of the Pannexin1-inhibitor Brilliant Blue FCF on Collagen-induced Aggregation
09:13

Turbidimetry on Human Washed Platelets: The Effect of the Pannexin1-inhibitor Brilliant Blue FCF on Collagen-induced Aggregation

Published on: April 6, 2017

  • Identification and classification of various inhibitor families.
  • Main Results:

    • Diverse salivary inhibitors identified, including apyrases, collagen-binding proteins, antithrombins, and disintegrins.
    • Enzymes like metalloproteases and PAF phosphorylcholine hydrolase block platelet aggregation.
    • Prostaglandins, adenosine, and nitric oxide-carrying proteins also exhibit antihemostatic properties.

    Conclusions:

    • Hematophagous salivary secretions (sialogenins) are rich in antihemostatic molecules.
    • These molecules target various pathways of platelet aggregation.
    • Sialogenins serve as valuable tools in research and hold therapeutic promise.