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This sustained ROS elevation ultimately functions as a potent inducer of autophagy 35

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(2) treatment with a pharmacological sEH inhibitor prevented AAA formation in conjunction with diminished expression of liver-derived inflammatory mediators, (3) accumulation of liver-derived pro-inflammatory mediators in the aorta is prevented by pharmacological sEH inhibition or hepatocyte-specific sEH gene disruption, (4) hepatocyte-specific sEH KO mice are protected against AAA formation
