New insight in aetiopathogenesis of aortic diseases.

Details

Serval ID
serval:BIB_612B6E905D94
Type
Article: article from journal or magazin.
Publication sub-type
Review (review): journal as complete as possible of one specific subject, written based on exhaustive analyses from published work.
Collection
Publications
Institution
Title
New insight in aetiopathogenesis of aortic diseases.
Journal
European Journal of Vascular Endovascular Surgery
Author(s)
Allaire E., Schneider F., Saucy F., Dai J., Cochennec F., Michineau S., Zidi M., Becquemin J.P., Kirsch M., Gervais M.
ISSN
1532-2165[electronic]
Publication state
Published
Issued date
2009
Volume
37
Number
5
Pages
531-537
Language
english
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't ; Review
Abstract
BACKGROUND: Knowledge in the aetiopathogeny of aortic disease helps to characterise aortic lesions better and determine the risk of evolution and therapeutic strategies as well. This article focusses on aneurysms and dissections, and excludes causes related to infection, systemic inflammatory diseases and trauma. METHODS AND RESULTS: The biomedical literature of the past 10 years has been reviewed here. Aortic diseases are heterogeneous along the aorta as far as their genetic determinants, contribution of smooth muscle cells, inflammation and thrombus formation are concerned. Degradation of extracellular matrix by proteases causing aortic disease is a 'terminal' event, modulated by genetic background, haemodynamic strain, cellular events and thrombus formation. New genetic determinants of aortic disease have been identified. Proteases degrading the aortic wall are derived from a variety of cell types in addition to macrophages, including neutrophils on the luminal thrombus, mesenchymal and endothelial cells in the wall. Smooth muscle cells contribute to aortic wall homeostasis against inflammation and proteolysis. The degradation of the wall is followed by, or paralleled with, a failure of aortic reconstruction. CONCLUSIONS: Aortic diseases are diverse, and involve a multiplicity of biological systems in the vascular wall and at the interface with blood. Future research needs to unravel distinct cellular and molecular mechanisms causing the clinical events, in particular, dissection, expansion of already formed aneurysms and rupture.
Keywords
Aneurysm, Dissecting/diagnosis, Aneurysm, Dissecting/etiology, Animals, Aortic Aneurysm/diagnosis, Aortic Aneurysm/etiology, Aortic Diseases/diagnosis, Aortic Diseases/etiology, Disease Progression, Humans, Leukocytes/metabolism, Leukocytes/pathology, Muscle, Smooth, Vascular/metabolism, Muscle, Smooth, Vascular/pathology, Peptide Hydrolases/biosynthesis
Pubmed
Web of science
Open Access
Yes
Create date
12/01/2010 15:48
Last modification date
20/08/2019 14:18
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