Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

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

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...

Peripheral Artery Disease III: Interprofessional Care

Peripheral Artery Disease III: Interprofessional Care

Peripheral Artery Disease (PAD) is characterized by narrowed arteries that diminish blood flow to the extremities. Effective management of PAD requires an interprofessional approach involving various healthcare professionals. The critical aspects of interprofessional care for PAD patients focus on risk factor modification, drug therapy, exercise therapy, nutrition therapy, critical limb ischemia care, and interventional radiology and surgical procedures.The primary treatment goal for PAD...

Formation of the Platelet Plug

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...

Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists

Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists

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...

Atherosclerosis III: Management

Atherosclerosis III: Management

Management of atherosclerosis involves an integrated strategy encompassing pharmacological treatment, surgical interventions, lifestyle changes, and nutrition therapy to address the multifactorial nature of the disease.Pharmacological TherapyA cornerstone of atherosclerosis management is the use of pharmacological agents. Statins, such as atorvastatin, are pivotal in inhibiting HMG-CoA reductase, an enzyme that catalyzes an initial step in cholesterol synthesis in the liver. This reduction in...

Anticoagulant Drugs: Low-Molecular-Weight Heparins

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

Australasian chronic lymphocytic leukaemia consensus statement: 2026 update.

Internal medicine journal·2026

Same author

Phase 3 PERSPECTIVE study: Ibrutinib with rituximab for initial treatment of patients with follicular lymphoma.

HemaSphere·2026

Same author

Significant variations in first-line mantle cell lymphoma care-an Australasian Lymphoma and Related Diseases Registry study.

Leukemia & lymphoma·2026

Same author

Leveraging technology to improve care: a real-time electronic dashboard within an anticoagulation stewardship service to optimise anticoagulant safety.

Journal of thrombosis and thrombolysis·2026

Same author

Obstetric and Gynaecologic Considerations in Inherited Bleeding Disorders.

Haemophilia : the official journal of the World Federation of Hemophilia·2026

Same author

Historical outcomes for patients with stage IA NLPHL: RGlobal nLPHL One Working Group (GLOW) retrospective analyses.

Blood advances·2026

Search research articles

Related Experiment Video

Updated: May 13, 2026

Ferric Chloride-induced Murine Thrombosis Models

Ferric Chloride-induced Murine Thrombosis Models

Published on: September 5, 2016

Antiplatelet therapy: present status and future prospects.

Justin R Hamilton¹, Zane Kaplan, Shaun P Jackson

¹Australian Centre for Blood Diseases, Monash University, 6th Level, Burnet Building, AMREP Campus, 89 Commercial Road, Melbourne, Victoria 3004, Australia +61 3 9903 0122 ; +61 3 9903 0228 ; Justin.Hamilton@med.monash.edu.au.

Expert Opinion on Drug Discovery

|March 15, 2013

Summary

Platelet accumulation causes arterial thrombosis, leading to heart attacks and strokes. Current antiplatelet therapies aim to improve treatment safety and effectiveness for cardiovascular disease management.

More Related Videos

Dynamic Multiparameter Platelet Function Assessment Using a Capacitive Biosensor

Dynamic Multiparameter Platelet Function Assessment Using a Capacitive Biosensor

Published on: May 2, 2025

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

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: May 13, 2026

Ferric Chloride-induced Murine Thrombosis Models

Ferric Chloride-induced Murine Thrombosis Models

Published on: September 5, 2016

Dynamic Multiparameter Platelet Function Assessment Using a Capacitive Biosensor

Dynamic Multiparameter Platelet Function Assessment Using a Capacitive Biosensor

Published on: May 2, 2025

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

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

Published on: April 6, 2017

Area of Science:

Cardiovascular Science
Hematology
Pharmacology

Background:

Platelet accumulation at vascular injury sites drives arterial thrombosis.
Arterial thrombosis underlies acute coronary syndromes and ischemic stroke, major causes of death.
Platelets are a primary therapeutic target in cardiovascular disease management.

Purpose of the Study:

To review the current landscape of antiplatelet therapy.
To explore future strategies for enhancing antiplatelet agent safety and efficacy.

Main Methods:

Literature review and perspective synthesis.
Analysis of current antiplatelet drug classes.
Discussion of emerging therapeutic approaches.

Main Results:

Antiplatelet therapy is crucial but faces challenges in balancing efficacy and bleeding risk.
Existing agents target various platelet activation pathways.
Novel strategies are being developed to optimize therapeutic outcomes.

Conclusions:

Antiplatelet therapy remains a cornerstone in managing thrombotic cardiovascular diseases.
Future directions focus on personalized medicine and improved safety profiles.
Optimizing antiplatelet strategies is essential for reducing morbidity and mortality.