title: [Pathobiology of idiopathic ascending aortic aneurysms].
abstract: BACKGROUND
  The majority of ascending aortic aneurysms cannot be related to any specific etiology and should be qualified as idiopathic. The incidence of this disease is increasing in the population of the developed countries but its pathobiology is poorly understood.
  
  
  OBJECTIVE
  This article is reviewing the publications concerning the pathobiology of idiopathic ascending aortic aneurysms.
  
  
  METHODS
  A PubMed search on articles published in English or French, between January 1965 and December 2007, on key-words << aortic root >>, << ascending aorta >>, << aortic arch >>, << thoracic aorta >>, << aneurysm >>, << dilatation >> and << dissection >> was undertaken. Articles on aneurysms related to inflammatory and infectious diseases, congenital or genetic syndromes were excluded.
  
  
  RESULTS
  The presented data suggests that destructive remodeling of the aortic wall, inflammation and angiogenesis, biomechanical wall stress, and molecular genetics are relevant mechanisms of idiopathic ascending aortic aneurysm formation and progression.
  
  
  CONCLUSIONS
  Sparse data available from few direct studies offer limited knowledge on pathobiology of idiopathic ascending aortic aneurysms.
  
  
  CONCLUSIONS
  A more intimate knowledge of the triggers and perpetrating factors of this disease might offer new diagnostic and treatment options.
authors.affiliation: CNRS UMR 7054, Centre de Recherches Chirurgicales << Dominique Chopin >>, Université Paris XII, Hôpital Henri Mondor, Créteil, France. ncostin.radu@gmail.com
authors.forename: N Costin
authors.initials: NC
authors.lastname: Radu
authors.forename: Marianne
authors.initials: M
authors.lastname: Gervais
authors.forename: Eric
authors.initials: E
authors.lastname: Allaire
authors.forename: Daniel Y
authors.initials: DY
authors.lastname: Loisance
authors.forename: Matthias E
authors.initials: ME
authors.lastname: Kirsch
mesh_terms: D001011:Aorta / Q000378:metabolism / Q000503:physiopathology*; D017545:Aortic Aneurysm, Thoracic / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D001019:Aortic Rupture / Q000453:epidemiology; D003094:Collagen / Q000378:metabolism; D004547:Elastic Tissue / Q000378:metabolism; D005838:Genotype; D006025:Glycosaminoglycans / Q000378:metabolism; D006801:Humans; D015151:Immunoblotting; D020781:Matrix Metalloproteinase 1 / Q000378:metabolism; D053509:Matrix Metalloproteinase 13 / Q000378:metabolism; D020783:Matrix Metalloproteinase 7 / Q000378:metabolism; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism; D020411:Oligonucleotide Array Sequence Analysis; D017354:Point Mutation / Q000235:genetics
chemical_list: D006025:Glycosaminoglycans; D003094:Collagen; D053509:Matrix Metalloproteinase 13; D020783:Matrix Metalloproteinase 7; D020780:Matrix Metalloproteinase 9; D020781:Matrix Metalloproteinase 1