Mouse models of platelet function in vivo
Abstract
Much of our current knowledge about the molecular mechanisms responsible for platelet activation and thrombin generation comes from in vitro studies where system components were examined in isolation. However, a comprehensive understanding of the hemostatic system requires study of how the various cellular and molecular components are integrated within, and influenced by, the dynamic physical environment present at sites of vascular injury in vivo. In this regard, animal models have played an integral role in studies of platelet biology since Bizzozero first recognized “blutplattchen” (i.e., platelets) as the cellular element of blood that responds to vascular injury in 1881 [1,2]. Current approaches take advantage of genetically modified mice to study molecular mechanisms within complex physiologic milieus. A variety of mechanisms for eliciting a hemostatic or thrombotic response in mice have been developed, and most have been adapted for use in multiple vascular beds. This review series explores several of these vascular injury models, with a particular emphasis on the mechanisms of injury and their relationship to events as they might occur in humans. As this review series focuses on mouse hemostasis and thrombosis models, it is worth noting at the outset that several important differences in the hemostatic system of mice and humans have been identified. Two obvious examples are platelet size and count (mouse platelets are smaller and more numerous) [3]. At the molecular…
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Evidence Hub reads this as a review, done in animal, not in people. Its evidence level is 5 of 5 (Very low · case / narrative / animal / in vitro / in silico). Case reports, narrative reviews, and animal, cell or computer-model studies give the weakest evidence for human health.
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