The expression of PGE2 is associated with the pathogenesis of human AAAs. Its expression is localized to macrophage-like cells within the inflammatory infiltrate and is controlled by the cox2 isoform of cyclooxygenase. Cox2 is, therefore, a potential target for pharmacotherapy of AAAs.

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Indomethacin attenuates aneurysm growth, and its effects are mediated via inhibition of the cox2 isoform of cyclooxygenase, which decreases PGE2 and MMP-9 synthesis.

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AAA and AIOD are associated with increased expression of the proinflammatory cytokines PGE2 and IL-6. However, AIOD is associated with a much higher level of IL-6 expression than is AAA, although the level of PGE2 expression is the same. This differential expression of IL-6 may help explain the pathogenesis of these 2 distinct aortic diseases.