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

572
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...
572
Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

782
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...
782
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists01:23

Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists

229
Prostacyclin receptor agonists are a class of therapeutic agents integral to managing pulmonary arterial hypertension (PAH). These drugs operate by mimicking the action of prostaglandin I2, or PGI2, a naturally occurring compound in the body.
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
229
Drugs that Destabilize Microtubules01:10

Drugs that Destabilize Microtubules

2.0K
Microtubules are dynamic structures and can be regulated by microtubule targeting agents (MTAs). Microtubule destabilizing drugs are a class of MTAs that destabilize and prevent microtubules' polymerization. Both natural and synthetic chemicals can be found under this class of drugs. Vincristine and vinblastine, two vinca alkaloids, and colchicine were among the first to be discovered. These drugs can affect cells in various ways, either by inducing a change in cell morphology, preventing...
2.0K
Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants01:18

Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants

1.3K
Oral anticoagulants are vital tools in preventing and treating blood clotting disorders. This diverse class of medications can be categorized as vitamin K antagonists, exemplified by warfarin, and direct thrombin inhibitors (DTIs), such as dabigatran, as well as factor Xa inhibitors, including rivaroxaban.
Warfarin, a prominent vitamin K antagonist family member, exerts its effect by inhibiting the enzyme VKORC1 (vitamin K epoxide reductase complex 1). By hindering this enzyme, warfarin...
1.3K
Treatment for Pulmonary Arterial Hypertension: Receptor Tyrosine Kinase Inhibitors and Calcium Channel Blockers01:26

Treatment for Pulmonary Arterial Hypertension: Receptor Tyrosine Kinase Inhibitors and Calcium Channel Blockers

215
Receptor tyrosine kinase inhibitors (TKIs) and calcium channel blockers (CCBs) are two critical categories of drugs employed in the treatment of pulmonary artery hypertension (PAH). PAH is a disease that causes high blood pressure in the pulmonary arteries, resulting in chest pain, fatigue, and shortness of breath.
TKIs, such as imatinib (Gleevec), are particularly effective in tackling the growth and mitogenic factors that become upregulated in PAH patients. These factors contribute to the...
215

You might also read

Related Articles

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

Sort by
Same author

Dried Blood Spot: A Tool to Ensure Broad Access to Hepatitis D Screening, Diagnosis, and Treatment Monitoring.

Liver international : official journal of the International Association for the Study of the Liver·2026
Same author

Real-world emergence of nirsevimab resistance in breakthrough infections with respiratory syncytial virus-B: a multicentre observational study in France.

The Lancet. Microbe·2026
Same author

Prospective multicentre study of upper respiratory mucosal transcriptomics reveals two major endotypes of critically ill COVID-19 patients.

Communications medicine·2026
Same author

Indeterminate Phase/Grey Zone of Chronic Hepatitis B: Clinical Features, Outcomes and Molecular Insights.

Liver international : official journal of the International Association for the Study of the Liver·2026
Same author

Hepatitis C virus elimination: So close, so far?

Antiviral research·2026
Same author

Hepatitis D Virus Seroconversion Rate Among People With Chronic Hepatitis B Virus Infection in France and The Gambia (Inci-D).

Open forum infectious diseases·2026

Related Experiment Video

Updated: Aug 1, 2025

Procoagulant Platelet Characterization by Measuring Phosphatidylserine Exposure and Microvesicle Release from Human Purified Platelets
05:49

Procoagulant Platelet Characterization by Measuring Phosphatidylserine Exposure and Microvesicle Release from Human Purified Platelets

Published on: November 29, 2024

658

Small-Molecule Cyclophilin Inhibitors Potently Reduce Platelet Procoagulant Activity.

Jens Van Bael1, Aline Vandenbulcke1, Abdelhakim Ahmed-Belkacem2

  • 1Laboratory for Thrombosis Research, KU Leuven Kulak Kortrijk Campus, 8500 Kortrijk, Belgium.

International Journal of Molecular Sciences
|April 28, 2023
PubMed
Summary
This summary is machine-generated.

Novel small-molecule cyclophilin inhibitors (SMCypIs) effectively reduce procoagulant platelets, a key factor in thrombosis. This targeted approach limits thrombosis without impairing normal platelet function, offering a promising therapeutic strategy.

Keywords:
Cyclophilin Dmitochondriaphosphatidylserineplateletsprocoagulantthrombosis

More Related Videos

Microfluidics in Assessing Platelet Function
06:47

Microfluidics in Assessing Platelet Function

Published on: November 8, 2024

978
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

12.1K

Related Experiment Videos

Last Updated: Aug 1, 2025

Procoagulant Platelet Characterization by Measuring Phosphatidylserine Exposure and Microvesicle Release from Human Purified Platelets
05:49

Procoagulant Platelet Characterization by Measuring Phosphatidylserine Exposure and Microvesicle Release from Human Purified Platelets

Published on: November 29, 2024

658
Microfluidics in Assessing Platelet Function
06:47

Microfluidics in Assessing Platelet Function

Published on: November 8, 2024

978
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

12.1K

Area of Science:

  • Cardiovascular Biology
  • Hematology
  • Pharmacology

Background:

  • Procoagulant platelets elevate thrombosis risk.
  • Cyclophilin D (CypD) mediates procoagulant platelet formation via mitochondrial permeability transition pore opening.
  • Inhibiting CypD is a potential antithrombotic strategy.

Purpose of the Study:

  • To evaluate novel small-molecule cyclophilin inhibitors (SMCypIs) for antithrombotic potential.
  • To compare SMCypIs with Cyclosporin A (CsA) in vitro.
  • To assess the impact of SMCypIs on platelet function and procoagulant activity.

Main Methods:

  • Investigated SMCypIs and CsA in vitro.
  • Assessed phosphatidylserine (PS) exposure and mitochondrial membrane potential loss.
  • Measured clotting time, fibrin formation under flow, P-selectin expression, integrin αIIbβ3 activation, and Adenosine 5'-diphosphate (ADP)-induced platelet aggregation.

Main Results:

  • SMCypIs significantly decreased procoagulant platelet formation and mitochondrial dysfunction.
  • SMCypIs reduced clotting time and fibrin formation, comparable to CsA.
  • SMCypIs did not affect normal platelet activation (P-selectin, αIIbβ3) or ADP-induced aggregation, unlike CsA.

Conclusions:

  • Specific cyclophilin inhibition with SMCypIs reduces procoagulant platelets without impairing normal platelet function.
  • SMCypIs represent a promising strategy for limiting thrombosis by targeting procoagulant platelet activity.