Document Detail

Beta-adrenoceptor signaling pathways mediate cardiac pathological remodeling.
MedLine Citation:
PMID:  22201979     Owner:  NLM     Status:  In-Data-Review    
Beta-adrenoceptors (ARs), members of the G protein-coupled receptor (GPCR) superfamily, play a key role in the rapid regulation of myocardial function. Meanwhile, chronic catecholamine stimulation of adrenoceptors has been proved to be involved in the adverse myocardial remodeling, including cardiac hypertrophy, fibrosis, and apoptosis, which finally develop into heart failure. In the clinical situation, sympathetic hyperactivity is a key factor in the development of heart failure, and beta-blockers greatly improve the outcome of the disease. However, heart failure is still one of the leading causes of death. Therefore, a full understanding of the mechanism of beta-AR-mediated cardiac remodeling could indicate more targets for treating heart failure. This review summarizes a number of important signaling pathways involved in the process of cardiac pathological remodeling under chronic adrenergic stimulation.
Yongnan Fu; Han Xiao; Youyi Zhang
Related Documents :
9550589 - The treatment of heart failure: the role of neurohumoral activation.
9008689 - Diastolic heart failure. what primary care physicians need to know.
10093769 - Heart failure.
16863479 - Management of acute decompensated heart failure: treatment, controversy, and future dir...
1644089 - Chagas cardiomyopathy and captopril.
8241009 - The management of heart failure: a matter of definition?
22132159 - Astrocyte proliferation following stroke in the mouse depends on distance from the infa...
9821079 - Myocarditis: a review.
629279 - Mid-systolic click and mitral valve prolapse following mitral commissurotomy.
Publication Detail:
Type:  Journal Article     Date:  2012-01-01
Journal Detail:
Title:  Frontiers in bioscience (Elite edition)     Volume:  4     ISSN:  1945-0508     ISO Abbreviation:  Front Biosci (Elite Ed)     Publication Date:  2012  
Date Detail:
Created Date:  2011-12-28     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101485240     Medline TA:  Front Biosci (Elite Ed)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1625-37     Citation Subset:  IM    
Institute of Vascular Medicine, Peking University Third Hospital and Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Beijing 100191, PR China.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms

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

Previous Document:  Antler regrowth as a form of epimorphic regeneration in vertebrates - a comparative view.
Next Document:  Inflammatory bowel disease: review and future view.