Document Detail

Involvement of the renin-angiotensin system in abdominal and thoracic aortic aneurysms.
MedLine Citation:
PMID:  22788237     Owner:  NLM     Status:  In-Data-Review    
Aortic aneurysms are relatively common maladies that may lead to the devastating consequence of aortic rupture. AAAs (abdominal aortic aneurysms) and TAAs (thoracic aortic aneurysms) are two common forms of aneurysmal diseases in humans that appear to have distinct pathologies and mechanisms. Despite this divergence, there are numerous and consistent demonstrations that overactivation of the RAS (renin-angiotensin system) promotes both AAAs and TAAs in animal models. For example, in mice, both AAAs and TAAs are formed during infusion of AngII (angiotensin II), the major bioactive peptide in the RAS. There are many proposed mechanisms by which the RAS initiates and perpetuates aortic aneurysms, including effects of AngII on a diverse array of cell types and mediators. These experimental findings are complemented in humans by genetic association studies and retrospective analyses of clinical data that generally support a role of the RAS in both AAAs and TAAs. Given the lack of a validated pharmacological therapy for any form of aortic aneurysm, there is a pressing need to determine whether the consistent findings on the role of the RAS in animal models are translatable to humans afflicted with these diseases. The present review compiles the recent literature that has shown the RAS as a critical component in the pathogenesis of aortic aneurysms.
Hong Lu; Debra L Rateri; Dennis Bruemmer; Lisa A Cassis; Alan Daugherty
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Clinical science (London, England : 1979)     Volume:  123     ISSN:  1470-8736     ISO Abbreviation:  Clin. Sci.     Publication Date:  2012 Nov 
Date Detail:
Created Date:  2012-07-13     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7905731     Medline TA:  Clin Sci (Lond)     Country:  England    
Other Details:
Languages:  eng     Pagination:  531-43     Citation Subset:  IM    
*Saha Cardiovascular Research Center, University of Kentucky, Lexington, KY 40536, U.S.A.
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