title: Humanizing thrombi in mice.
abstract: Antiplatelet therapies form the cornerstone of atherothrombosis prevention, reducing the morbidity and mortality associated with cardiovascular disease. Despite these benefits, there is still an unmet need for more effective and safer pharmacological agents. To expedite this process, biological platforms that better reflect the intravascular environment in humans will be required in order to shorten drug development time, enable better determination of dosing regimes, and aid in the design of clinical studies. This article focuses on a unique genetically modified animal model that predicts the in vivo response of antiplatelet agents in humans more accurately than is currently possible using conventional murine models of thrombosis.
authors.affiliation: Division of Cardiology, Department of Medicine, Columbia University Medical Center, New York, NY 10032, USA.
authors.forename: Jorge
authors.initials: J
authors.lastname: Magallon
authors.forename: Matthew
authors.initials: M
authors.lastname: Egalka
authors.forename: Thomas G
authors.initials: TG
authors.lastname: Diacovo
mesh_terms: D000818:Animals; D001777:Blood Coagulation / Q000187:drug effects / Q000235:genetics*; D004195:Disease Models, Animal; D005343:Fibrinolytic Agents / Q000494:pharmacology; D020022:Genetic Predisposition to Disease; D006801:Humans; D051379:Mice; D008822:Mice, Transgenic; D010641:Phenotype; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology; D017354:Point Mutation; D013045:Species Specificity; D013927:Thrombosis / Q000097:blood / Q000235:genetics* / Q000517:prevention & control; D014841:von Willebrand Factor / Q000235:genetics* / Q000378:metabolism
chemical_list: D005343:Fibrinolytic Agents; D010975:Platelet Aggregation Inhibitors; D014841:von Willebrand Factor