Key result
Mouse models of thrombosis demonstrate that the cellular sources of tissue factor driving thrombogenesis are highly model-dependent, necessitating rigorous controls in future studies.
The cellular source of tissue factor driving thrombosis in mouse models is highly dependent on the specific injury model used, necessitating rigorous controls in future studies.
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Urges caution extrapolating mouse thrombosis data to patients; leaves open identification of relevant human cellular sources.
Mouse models of thrombosis have extended our understanding of the role of tissue factor (TF) in thrombogenesis. Because tissue factor deficiency is embryonic lethal in mice, inventive genetic models are required to probe the role of TF in thrombosis. TF is expressed by different cell types, including vascular smooth muscle cells, cardiomyocytes, fibroblasts, and monocytes. Platelets and endothelial cells also express TF under certain conditions, but the importance of this TF remains controversial. Animal models are commonly used to evaluate the contribution of TF from each cell type to thrombogenesis. Although a variety of well-established injury techniques are used to induce thrombosis, it is likely that the sources of TF that drive thrombosis are model dependent. Therefore, rigorous controls are needed before thrombogenesis can be attributed to TF from a particular cell type. This review summarizes data from mouse models that have attempted to delineate the role of TF in thrombus formation in response to various types of vascular injury. We have consolidated this information to generate unifying concepts that require testing in future studies.
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Kretz et al. (2010) conducted a review in Thrombosis. Tissue factor was evaluated. Mouse models of thrombosis demonstrate that the cellular sources of tissue factor driving thrombogenesis are highly model-dependent, necessitating rigorous controls in future studies.
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