Abstract: Chronic activation of the ?-Adrenergic Receptor (?-AR) can have deleterious effects on the heart, and animal models over-expressing the ?-AR develop heart failure. In the classical ?-AR pathway, activation of the receptor results in increased cyclic AMP (cAMP) levels. However, ?-ARs are desensitized in the failing heart and cAMP levels are decreased. Phosphodiesterase 3A (PDE3A) hydrolyzes cAMP in certain subcellular compartments in cardiac myocytes, regulating cAMP levels and subsequent protein kinase A mediated cell signaling. By virtue of being freely diffusable intracellularly and being reduced in failing myocardial tissue, cAMP is reduced in certain important cardiac myocyte subcellular compartments such as the microdomain occupied by phospholamban.

Abstract: Embodiments of the invention are directed to identifying or treating a patient that would benefit from phosphodiesterase inhibitor therapy.

Abstract: Embodiments of the invention are directed to identifying or treating a patient that would benefit from phosphodiesterase inhibitor therapy.

Abstract: Provided are methods of treating heart failure in children using B1-selective adrenergic receptor antagonists, alone or in combination with other agents, including B-2-selective adrenergic receptor agonists.

Abstract: Chronic activation of the ?-Adrenergic Receptor (?-AR) can have deleterious effects on the heart, and animal models over-expressing the ?-AR develop heart failure. In the classical ?-AR pathway, activation of the receptor results in increased cyclic AMP(cAMP) levels. However, ?-ARs are desensitized in the failing heart and cAMP levels are decreased. Phosphodiesterase 3A (PDE3A) hydrolyzes cAMP in certain subcellular compartments in cardiac myocytes, regulating cAMP levels and subsequent protein kinase A mediated cell signaling. By virtue of being freely diffusable intracellularly and being reduced in failing myocardial tissue, cAMP is reduced in certain important cardiac myocyte subcellular compartments such as the microdomain occupied by phospholamban.

Abstract: The present invention discloses specific miRNAs as novel biomarkers and therapeutic targets in the treatment of heart failure. Methods of treating or preventing heart failure in a subject by administering mimics or inhibitors of these particular miRNAs are disclosed. A method of diagnosing or prognosing heart failure in a subject by determining the level of expression of one or more miRNAs is also described.

Abstract: The present invention provides for methods of predicting progression of pediatric heart failure using miRNA biomarkers, as well as subsequent treatment of patients based on their classification.

Abstract: Provided are methods of treating heart failure in children using B1-selective adrenergic receptor antagonists, alone or in combination with other agents, including B-2-selective adrenergic receptor agonists.

Abstract: Embodiments of the invention are directed to identifying or treating a patient that would benefit from phosphodiesterase inhibitor therapy.

Abstract: The present invention discloses specific miRNAs as novel biomarkers and therapeutic targets in the treatment of heart failure. Methods of treating or preventing heart failure in a subject by administering mimics or inhibitors of these particular miRNAs are disclosed. A method of diagnosing or prognosing heart failure in a subject by determining the level of expression of one or more miRNAs is also described.

Abstract: The present invention provides for methods of treating and preventing cardiovascular diseases, in particular pathological cardiac hypertrophy and chronic heart failure, by applying an inhibitor of Ku. The present invention also provides for methods of screening to find inhibitors of Ku and inhibitors of cardiac hypertrophy and heart failure.