Reversal of cardiac remodeling by modulation of adrenergic receptors: a new frontier in heart failure.
OBJECTIVE
Heart failure is a common clinical syndrome, and despite intensive medical therapy it remains a leading cause of global morbidity and mortality. Pathological stimuli promote a general remodeling process in the heart.


RESULTS
Recent animal studies have highlighted very promising novel therapeutic possibilities, based on the regulation of adrenergic receptor function, and novel signaling pathways are being discovered that could be relevant for future molecular approaches.


CONCLUSIONS
This review highlights some of the novel approaches to reverse pathological remodeling and improve cardiac dysfunction, placing emphasis on strategies targeting the adrenergic receptors.
Perrino
Cinzia
C
Division of Cardiology, Department of Clinical Medicine, Cardiovascular and Immunological Sciences, Federico II University, Naples, Italy.
Rockman
Howard A
HA
D000322:Adrenergic Agonists / Q000494:pharmacology; D018674:Adrenergic Antagonists / Q000494:pharmacology; D000818:Animals; D006332:Cardiomegaly / Q000503:physiopathology; D054769:G-Protein-Coupled Receptor Kinase 2 / Q000502:physiology; D020555:GTP-Binding Protein Regulators / Q000502:physiology*; D006333:Heart Failure / Q000188:drug therapy / Q000503:physiopathology*; D006801:Humans; D051379:Mice; D019869:Phosphatidylinositol 3-Kinases / Q000502:physiology; D011941:Receptors, Adrenergic / Q000235:genetics / Q000502:physiology*; D020257:Ventricular Remodeling / Q000187:drug effects / Q000502:physiology*
D000322:Adrenergic Agonists; D018674:Adrenergic Antagonists; D020555:GTP-Binding Protein Regulators; D011941:Receptors, Adrenergic; D019869:Phosphatidylinositol 3-Kinases; D054769:G-Protein-Coupled Receptor Kinase 2