TGFB1 and hypertensive disorder: The vulnerable aorta phenotype resulting from disruption of TGF-β signaling and sensitizing to dissection elicited by transient and sustained elevations in blood pressure provides a mechanism and experimental confirmation of recent computational modeling that hypertension exacerbates but does not initiate focal mural defects leading to aortopathy, and that continual ECM turnover, either balanced or unbalanced, is required for progressive aortic disease (63).