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

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...

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...

Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants

Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants

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...

Antihypertensive Drugs: Angiotensin II Receptor Blockers

Antihypertensive Drugs: Angiotensin II Receptor Blockers

In the renin-angiotensin-aldosterone system, a hormone called angiotensin II plays a crucial role. It binds to the AT1 receptors in vascular smooth muscles coupled with Gq proteins. The activation of these receptors activates an enzyme called phospholipase C, which releases two molecules: inositol trisphosphate and diacylglycerol. These molecules cause a chain reaction that leads to the phosphorylation of myosin light chains and promotes interaction between actin and myosin, leading to smooth...

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...

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...

You might also read

Related Articles

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

Sort by

Same author

Controlling tosylation versus chlorination during end group modification of PCL.

European polymer journal·2026

Same author

Advances in Additive Manufactured Scaffolds Mimicking the Osteochondral Interface.

Advanced nanobiomed research·2026

Same author

Transformative microsystems for Cancer Diagnosis, treatment monitoring, and clinical integration: Outcomes from an NCI Workshop.

Journal of the National Cancer Institute·2026

Same author

Artificial intelligence in cancer diagnostics: a primer for clinicians and scientists.

Journal of the National Cancer Institute·2026

Same author

Long-term disinfection of 3D-printed denture resin: physical and biological in vitro assessments.

Journal of materials science. Materials in medicine·2026

Same author

Effect of surface polishing on roughness, biofilm formation, and biocompatibility of LCD-printed denture base polymer.

Scientific reports·2026

Search research articles

Related Experiment Video

Updated: Jun 16, 2026

Characterizing Modulators of Protease-Activated Receptors with a Calcium Mobilization Assay Using a Plate Reader

Characterizing Modulators of Protease-Activated Receptors with a Calcium Mobilization Assay Using a Plate Reader

Published on: May 24, 2024

ACE2 activation promotes antithrombotic activity.

Rodrigo A Fraga-Silva¹, Brian S Sorg, Mamta Wankhede

¹Department of Physiology and Functional Genomics, University of Florida, Gainesville, Florida 32610, United States of America.

Molecular Medicine (Cambridge, Mass.)

|January 30, 2010

Summary

Activating angiotensin-converting enzyme 2 (ACE2) protects against thrombosis. This study shows ACE2 activation reduces thrombus formation and platelet aggregation, suggesting ACE2 as a novel therapeutic target for thrombotic diseases.

More Related Videos

Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice

Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice

Published on: September 28, 2015

Ferric Chloride-induced Murine Thrombosis Models

Ferric Chloride-induced Murine Thrombosis Models

Published on: September 5, 2016

Related Experiment Videos

Last Updated: Jun 16, 2026

Characterizing Modulators of Protease-Activated Receptors with a Calcium Mobilization Assay Using a Plate Reader

Characterizing Modulators of Protease-Activated Receptors with a Calcium Mobilization Assay Using a Plate Reader

Published on: May 24, 2024

Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice

Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice

Published on: September 28, 2015

Ferric Chloride-induced Murine Thrombosis Models

Ferric Chloride-induced Murine Thrombosis Models

Published on: September 5, 2016

Area of Science:

Cardiovascular Biology
Thrombosis Research
Enzymology

Background:

The renin-angiotensin system plays a crucial role in cardiovascular homeostasis.
Dysregulation of angiotensin-converting enzyme 2 (ACE2) activity is implicated in thrombotic disorders.
The protective role of the ACE2/angiotensin-(1-7)/Mas receptor axis in thrombosis requires further investigation.

Purpose of the Study:

To evaluate the protective effects of a novel ACE2 activator (XNT) against thrombosis.
To test the hypothesis that activating the ACE2 axis can prevent thrombus formation.
To investigate the association between ACE2 activity and thrombus formation in spontaneously hypertensive rats (SHR).

Main Methods:

Thrombus induction in the vena cava of spontaneously hypertensive rats (SHR) and Wistar Kyoto (WKY) rats.
Measurement of ACE2 and ACE activity within thrombi.
Real-time thrombus formation visualization using intravital microscopy in nude mice.
Administration of ACE2 inhibitor (DX600) and ACE2 activator (XNT) to assess their effects on thrombus formation.

Main Results:

SHR exhibited significantly greater thrombus weight compared to WKY rats, associated with reduced thrombus ACE2 activity.
ACE2 inhibition (DX600) increased thrombus weight, while XNT treatment significantly attenuated thrombus formation in SHR.
XNT treatment reduced platelet attachment to injured vessels, decreased thrombus size, and prolonged occlusion time in mice.

Conclusions:

Decreased thrombus ACE2 activity is linked to enhanced thrombus formation in SHR.
Activation of ACE2 by XNT effectively attenuates thrombus formation and reduces platelet aggregation.
The ACE2 pathway represents a promising therapeutic target for managing thrombotic diseases.