Aging induces endothelial dysfunction while sparing arterial thrombosis.
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.
Stämpfli
Simon F
SF
Cardiovascular Research, Institute of Physiology, University of Zurich, Zurich, Switzerland.
Akhmedov
Alexander
A
Gebhard
Cathérine
C
Lohmann
Christine
C
Holy
Erik W
EW
Rozenberg
Izabela
I
Spescha
Remo
R
Shi
Yi
Y
Lüscher
Thomas F
TF
Tanner
Felix C
FC
Camici
Giovanni G
GG
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
D017931:DNA Primers; D018836:Inflammation Mediators; D012333:RNA, Messenger; D013925:Thromboplastin; D020780:Matrix Metalloproteinase 9; C501830:Mmp9 protein, mouse