title: Aging induces endothelial dysfunction while sparing arterial thrombosis.
abstract: OBJECTIVE
  To assess the effects of aging on arterial thrombus formation by comparing 2-year-old with 11-week-old C57Bl6 mice.
  
  
  RESULTS
  Aging is a major risk factor for cardiovascular disease. In humans, assessing the direct effects of aging on vascular homeostasis is difficult because it occurs in the presence of other risk factors. Arterial thrombosis is the critical event in cardiovascular diseases; however, it is not known whether aging per se promotes its occurrence. Mice represent an interesting system to address this issue because they age without spontaneously developing other risk factors. Organ chamber experiments confirmed the advanced level of aging of old mice. As previously shown, old mice exhibited endothelial dysfunction; however, arterial thrombosis induced by photochemical injury was unchanged. Arterial tissue factor expression and activity; expressions of tissue factor pathway inhibitor, thrombomodulin, and plasminogen activator inhibitor 1; prothrombin time; partial thromboplastin time; thrombin-antithrombin complex; and platelet activation were comparable in both groups.
  
  
  CONCLUSIONS
  Although these results cannot be directly extrapolated to humans, this study contributes novel important information on the direct effect of aging on arterial thrombosis and underscores the importance of controlling modifiable risk factors in aged individuals.
authors.affiliation: Cardiovascular Research, Institute of Physiology, University of Zurich, Zurich, Switzerland.
authors.forename: Simon F
authors.initials: SF
authors.lastname: Stämpfli
authors.forename: Alexander
authors.initials: A
authors.lastname: Akhmedov
authors.forename: Cathérine
authors.initials: C
authors.lastname: Gebhard
authors.forename: Christine
authors.initials: C
authors.lastname: Lohmann
authors.forename: Erik W
authors.initials: EW
authors.lastname: Holy
authors.forename: Izabela
authors.initials: I
authors.lastname: Rozenberg
authors.forename: Remo
authors.initials: R
authors.lastname: Spescha
authors.forename: Yi
authors.initials: Y
authors.lastname: Shi
authors.forename: Thomas F
authors.initials: TF
authors.lastname: Lüscher
authors.forename: Felix C
authors.initials: FC
authors.lastname: Tanner
authors.forename: Giovanni G
authors.initials: GG
authors.lastname: Camici
mesh_terms: D000375:Aging / Q000235:genetics / Q000473:pathology* / Q000502:physiology*; D000818:Animals; D001013:Aorta, Thoracic / Q000473:pathology / Q000503:physiopathology; D001018:Aortic Diseases / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D001483:Base Sequence; D001777:Blood Coagulation; D001792:Blood Platelets / Q000502:physiology; D002341:Carotid Artery Thrombosis / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D017931:DNA Primers / Q000235:genetics; D004195:Disease Models, Animal; D004730:Endothelium, Vascular / Q000503:physiopathology*; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D008297:Male; D020780:Matrix Metalloproteinase 9 / Q000235:genetics / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D012307:Risk Factors; D013925:Thromboplastin / Q000235:genetics / Q000378:metabolism; D014664:Vasodilation
chemical_list: D017931:DNA Primers; D018836:Inflammation Mediators; D012333:RNA, Messenger; D013925:Thromboplastin; D020780:Matrix Metalloproteinase 9; C501830:Mmp9 protein, mouse