Document Detail


Mechanism of cardiac fibrosis by angiotensin. New insight revealed by genetic engineering.
MedLine Citation:
PMID:  10881748     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Accumulating data show that excess of angiotensin II (Ang II) is involved in cardiac fibrosis. Many experimental studies suggested that Ang II induces cardiac fibrosis not by its blood pressure-raising action, but rather by a direct action on the heart. However, it has been difficult to distinguish the local and systemic actions in vivo. Recent genetic technology sheds new light on this problem. This review focuses on the recent advances and newly arising issues regarding the mechanism of Ang II-induced cardiac fibrosis.
Authors:
T Matsusaka; H Katori; T Homma; I Ichikawa
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review    
Journal Detail:
Title:  Trends in cardiovascular medicine     Volume:  9     ISSN:  1050-1738     ISO Abbreviation:  Trends Cardiovasc. Med.     Publication Date:  1999 Oct 
Date Detail:
Created Date:  2000-08-09     Completed Date:  2000-08-09     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  9108337     Medline TA:  Trends Cardiovasc Med     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  180-4     Citation Subset:  IM    
Affiliation:
Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, TN, USA.
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MeSH Terms
Descriptor/Qualifier:
Angiotensin II / pharmacology*
Animals
Chimera
Fibrosis
Heart / drug effects*
Humans
Mice
Mice, Mutant Strains
Mice, Transgenic
Myocardium / metabolism,  pathology*
Receptors, Angiotensin / metabolism
Grant Support
ID/Acronym/Agency:
DK-37868/DK/NIDDK NIH HHS; DK-44757/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Receptors, Angiotensin; 11128-99-7/Angiotensin II

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


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