New insight in aetiopathogenesis of aortic diseases.
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.


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.
Allaire
E
E
Surgical Research Center, Paris 12 University, CNRS EAC 7054, 8 rue du Général Sarrail, 94010 Créteil Cedex, France.
Schneider
F
F
Saucy
F
F
Dai
J
J
Cochennec
F
F
Michineau
S
S
Zidi
M
M
Becquemin
J-P
JP
Kirsch
M
M
Gervais
M
M
D000784:Aortic Dissection / Q000175:diagnosis / Q000209:etiology / Q000628:therapy; D000818:Animals; D001014:Aortic Aneurysm / Q000175:diagnosis / Q000209:etiology / Q000628:therapy; D001018:Aortic Diseases / Q000175:diagnosis* / Q000209:etiology*; D018450:Disease Progression; D006801:Humans; D007962:Leukocytes / Q000378:metabolism / Q000473:pathology; D009131:Muscle, Smooth, Vascular / Q000378:metabolism / Q000473:pathology*; D010447:Peptide Hydrolases / Q000096:biosynthesis
D010447:Peptide Hydrolases