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Pressure overload induces cardiac hypertrophy, which often ends in heart failure. Afadin is an adaptor protein that is ubiquitously expressed and, in the heart, it localizes at intercalated disks. The current study aimed to examine the afadin-mediated cardiac phenotype in mice exposed to different types of pressure overload: transverse aortic constriction (TAC) burden and angiotensin II (Ang II) stimulation. Methods and Results : Conditional knockout mice with selective deletion of afadindoi:10.1253/circj.cj-17-0394 pmid:28659552 fatcat:hnfjdrv3ynfvvli7wdaxbd2deu