Our finding for the first time illustrates that Ang II, a well-documented risk factor for systemic hypertension and remodeling, pulmonary arterial hypertension, heart failure, myocardial infarction, aortic aneurysm, and inflammation (70), has the ability in an HFD-fed ApoE-KO background to bypass HFD-induced metabolic reprogramming and amplify inflammatory responses in the abdominal aorta but not the thoracic aorta. This evidence concerns the gene APOE and myocardial infarction.