Document Detail

Reversal of cardiac remodeling by modulation of adrenergic receptors: a new frontier in heart failure.
MedLine Citation:
PMID:  17762546     Owner:  NLM     Status:  MEDLINE    
PURPOSE OF REVIEW: 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. RECENT FINDINGS: 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. SUMMARY: This review highlights some of the novel approaches to reverse pathological remodeling and improve cardiac dysfunction, placing emphasis on strategies targeting the adrenergic receptors.
Cinzia Perrino; Howard A Rockman
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Current opinion in cardiology     Volume:  22     ISSN:  0268-4705     ISO Abbreviation:  Curr. Opin. Cardiol.     Publication Date:  2007 Sep 
Date Detail:
Created Date:  2007-08-31     Completed Date:  2007-11-29     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8608087     Medline TA:  Curr Opin Cardiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  443-9     Citation Subset:  IM    
Division of Cardiology, Department of Clinical Medicine, Cardiovascular and Immunological Sciences, Federico II University, Naples, Italy.
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MeSH Terms
1-Phosphatidylinositol 3-Kinase / physiology
Adrenergic Agonists / pharmacology
Adrenergic Antagonists / pharmacology
Cardiomegaly / physiopathology
G-Protein-Coupled Receptor Kinase 2 / physiology
GTP-Binding Protein Regulators / physiology*
Heart Failure / drug therapy,  physiopathology*
Receptors, Adrenergic / genetics,  physiology*
Ventricular Remodeling / drug effects,  physiology*
Reg. No./Substance:
0/Adrenergic Agonists; 0/Adrenergic Antagonists; 0/GTP-Binding Protein Regulators; 0/Receptors, Adrenergic; EC 3-Kinase; EC Receptor Kinase 2

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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