Background: An abdominal aortic aneurysm (AAA), which affects approximately 10% of
Japanese men aged ≥ 65 years, is frequently associated with hypertension, dyslipidemia, and other lifestyle-
related diseases. The development of an AAA is attributed to chronic inflammation concomitant
with arteriosclerotic changes. However, an accurate pathomechanism associated with AAA remains uncertain,
and questions such as why only a particular group/percentage of patients with arteriosclerosis develop
aneurysms and how diabetes suppresses aneurysm development remain unanswered.
Objective: We examined a novel mechanism to develop AAA based on histopathological findings following
analysis of the human AAA tissues. Additionally, based on these findings, we developed a new
animal model of AAA, in which the histopathological characteristics are similar to human AAA tissue.
Results: Recently, we identified stenosis of the vasa vasorum (VV) in aortic segments showing dilatation.
The aorta is the largest artery in our circulatory system. Under physiological conditions, the inner
layer of the aorta is nourished via direct diffusion of nutrients from the luminal blood flow, whereas
the outer adventitia is primarily perfused by the VV. Therefore, hypoperfusion of the VV induces hypoxia
and subsequent inflammation and tissue degeneration of the aortic wall, resulting in aneurysm
Based on these findings, we established an AAA animal model by reducing the blood flow through the
VV to the aortic wall. AAA was successfully reproduced in our animal model. Histopathological findings
in this model were indistinguishable from those observed in humans, and pronounced abnormality
in lipid composition in blood vessel adventitia was also observed.
Conclusion: Thus, hypoperfusion of the aortic wall appeared to be sufficient to cause inflammationinduced
AAA. These findings may provide potential targets for novel therapeutics for the management
of an AAA.