Hemodynamic stresses in the mouse aortic arch are larger and more uniform than in humans, challenging accepted models of hemodynamics in mouse atherogenesis.
Challenges direct translation of mouse aortic hemodynamics to human atherosclerosis; leaves open validity of murine models for atherogenesis research.
Mice are widely used to study arterial disease in humans, and the pathogenesis of arterial diseases is known to be strongly influenced by hemodynamic factors. It is, therefore, of interest to characterize the hemodynamic environment in the mouse arterial tree. Previous measurements have suggested that many relevant hemodynamic variables are similar between the mouse and the human. Here we use a combination of Doppler ultrasound and MRI measurements, coupled with numerical modeling techniques, to characterize the hemodynamic environment in the mouse aortic arch at high spatial resolution. We find that the hemodynamically induced stresses on arterial endothelial cells are much larger in magnitude and more spatially uniform in the mouse than in the human, an effect that can be explained by fluid mechanical scaling principles. This surprising finding seems to be at variance with currently accepted models of the role of hemodynamics in atherogenesis and the known distribution of atheromatous lesions in mice.
No takes yet. Share an insight, caveat, or question.
Feintuch et al. (2006) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: