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doi:10.1371/journal.pone.0003815

Gene set enrichment analysis of the PC1 loadings showed E2F and MYC targets and mTORC1 pathway genes in the top ten under both normoxic and hypoxic conditions, with hypoxia and glycolysis genes under normoxic conditions and oxidative phosphorylation, and epithelial mesenchymal transition genes under hypoxic conditions (Supplementary Table 4)

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Here, using a pharmacological antagonist of sEH and hepatocyte-specific Ephx2 (which encodes sEH ) knockout (KO) mice, and two distinct models of AAA formation, we investigated the role of hepatic sEH in the pathogenesis of AAA