Cardiac Dysfunction

Methods and Results—We studied the role of CREM in 1AR-mediated cardiac effects, comparing transgenic mice with heart-directed expression of 1AR in the absence and presence of functional CREM. CREM inactivation protected from cardiomyocyte hypertrophy, fibrosis, and left ventricular dysfunction in 1AR-overexpressing mice. Transcriptome and proteome analysis revealed a set of predicted CREB/CREM target genes including the cardiac ryanodine receptor,

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