Related Experiment Video

Updated: May 4, 2026

Ferric Chloride-induced Murine Thrombosis Models
10:37

Ferric Chloride-induced Murine Thrombosis Models

Published on: September 5, 2016

21.9K

Thrombomodulin--a new target for treating stroke at the crossroad of coagulation and inflammation

J Wenzel, J C Assmann, M Schwaninger1

  • 1Institute of Experimental and Clinical Pharmacology and Toxicology, University of Luebeck, Ratzeburger Allee 160, 23562 Luebeck, Germany. markus.schwaninger@pharma.uni-luebeck.de.

Current Medicinal Chemistry
|December 31, 2013
PubMed

Thrombomodulin (TM) is a membrane protein mainly expressed by endothelial cells. It is part of the anticoagulant protein C system but recently several effects were discovered which occur independently of protein C activation. TM binds thrombin and promotes the cleavage of protein C and the thrombin activatable fibrinolysis inhibitor (TAFI), thereby inhibiting coagulation and fibrinolysis. Additionally, it interferes with inflammation, stabilizes barrier function, and increases blood flow under pathological conditions. Recombinant soluble TM protects against tissue damage and partially restores normal function after ischemia in several organs. Recently, it was shown to reduce the infarct size in stroke models. Compared to other anticoagulant compounds the risk of bleeding seems to be smaller in animals and humans treated with soluble TM. With its multiple actions TM represents a new candidate for stroke treatment. In this review we focus on the effects of TM in coagulation, inflammation, and on its protective roles in the prevention of ischemic brain damage.

More Related Videos

Ferric Chloride-induced Thrombosis Mouse Model on Carotid Artery and Mesentery Vessel07:26

Ferric Chloride-induced Thrombosis Mouse Model on Carotid Artery and Mesentery Vessel

Published on: June 29, 2015

18.0K
A Fibrin-Enriched and tPA-Sensitive Photothrombotic Stroke Model09:42

A Fibrin-Enriched and tPA-Sensitive Photothrombotic Stroke Model

Published on: June 4, 2021

3.2K

Related Concept Videos

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...
2.6K
Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants01:18

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...
2.7K
Venous Thrombosis III: Interprofessional Care01:29

Venous Thrombosis III: Interprofessional Care

Venous thrombosis requires effective prevention and treatment strategies to improve patient outcomes and reduce potential complications.Prevention StrategiesHealthcare providers must prioritize preventing venous thromboembolism (VTE) for all adult patients upon admission. Interventions depend on bleeding and thrombosis risk, medical history, current medications, diagnoses, planned procedures, and patient preferences. Patients on bed rest should change positions every two hours and, if not...
482
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
30
Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
6.0K
Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which...
10.9K