Figure 4.
Figure 4. Quantification of atherosclerotic lesions area in aortas of wildtype (+/+), TP deficient (TP−/ −) and IP deficient (IP −/ −) mice on an apoE deficient background at 20 weeks of age. TP deficiency retarded and IP deficiency accelerated atherogenesis, suggesting that these mediators have opposing roles in atherosclerotic lesion development. Data are means ± SEM (n = 5 each). / (Redrawn with permission from Kobayashi T, Tahara Y, Matsumoto M, et al. Roles of thromboxane A2 and prostacyclin in the development of atherosclerosis in apoE-deficient mice. J Clin Invest. 2004;114(6):784–94.)

Quantification of atherosclerotic lesions area in aortas of wildtype (+/+), TP deficient (TP/) and IP deficient (IP/) mice on an apoE deficient background at 20 weeks of age. TP deficiency retarded and IP deficiency accelerated atherogenesis, suggesting that these mediators have opposing roles in atherosclerotic lesion development. Data are means ± SEM (n = 5 each).

(Redrawn with permission from Kobayashi T, Tahara Y, Matsumoto M, et al. Roles of thromboxane A2 and prostacyclin in the development of atherosclerosis in apoE-deficient mice.

J Clin Invest
.
2004
;
114
(6):
784
–94.
)

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