Plasminogen activator inhibitor (PAI)-1 in vascular inflammation and thrombosis

被引:113
作者
Aso, Yoshimasa [1 ]
机构
[1] Dokkyo Med Univ, Koshigaya Hosp, Dept Internal Med, Koshigaya, Saitama 3438555, Japan
来源
FRONTIERS IN BIOSCIENCE-LANDMARK | 2007年 / 12卷
关键词
plasminogen activator inhibitor 1; cardiovascular disease; atherothrombosis; type; 2; diabetes; metabolic syndrome; review;
D O I
10.2741/2285
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Impaired fibrinolysis may be associated with development of atherothrombotic cardiovascular disease ( CVD) in metabolic syndrome or type 2 diabetes. Plasma plasminogen activator inhibitor (PAI)-1, a potent inhibitor of fibrinolysis, is elevated in a number of clinical situations that are associated with high incidence of CVD. Impaired fibrinolysis resulting from high plasma PAI-1 can lead to excessive fibrin accumulation within vessels, resulting in atherothrombosis. Increased expression of PAI-1 is found in atherosclerotic lesions in humans, especially atherosclerotic plaques in patients with type 2 diabetes. This increased vascular expression of PAI-1 promotes neointima formation via accumulation of fibrin or fibrinogen as a result of inhibited clearance of platelet-fibrin thrombi. PAI-1, an acute phase protein, also could be involved in vascular inflammation. PAI-1 may be associated not only systemically but also locally with development of CVD.
引用
收藏
页码:2957 / 2966
页数:10
相关论文
共 98 条
[1]   Relationship of metabolic syndrome and fibrinolytic dysfunction to cardiovascular disease [J].
Anand, SS ;
Yi, QL ;
Gerstein, H ;
Lonn, E ;
Jacobs, R ;
Vuksan, V ;
Teo, K ;
Davis, B ;
Montague, P ;
Yusuf, S .
CIRCULATION, 2003, 108 (04) :420-425
[2]   DIURNAL-VARIATION OF TISSUE-TYPE PLASMINOGEN-ACTIVATOR AND ITS RAPID INHIBITOR (PAI-1) [J].
ANGLETON, P ;
CHANDLER, WL ;
SCHMER, G .
CIRCULATION, 1989, 79 (01) :101-106
[3]   Metabolic syndrome accompanied by hypercholesterolemia is strongly associated with proinflammatory state and impairment of fibrinolysis in patients with type 2 diabetes - Synergistic effects of plasminogen activator inhibitor-1 and thrombin-activatable fibrinolysis inhibitor [J].
Aso, Y ;
Wakabayashi, S ;
Yamamoto, R ;
Matsutomo, R ;
Takebayashi, K ;
Inukai, T .
DIABETES CARE, 2005, 28 (09) :2211-2216
[4]   Enhancement of fibrinolysis in poorly controlled, hospitalized type 2 diabetic patients by short-term metabolic control: Association with a decrease in plasminogen activator inhibitor 1 [J].
Aso, Y ;
Okumura, K ;
Yoshida, N ;
Tayama, K ;
Takemura, Y ;
Inukai, T .
EXPERIMENTAL AND CLINICAL ENDOCRINOLOGY & DIABETES, 2004, 112 (04) :175-180
[5]   Impaired fibrinolytic compensation for hypercoagulability in obese patients with type 2 diabetes: Association with increased plasminogen activator inhibitor-1 [J].
Aso, Y ;
Matsumoto, S ;
Fujiwara, Y ;
Tayama, K ;
Inukai, T ;
Takemura, Y .
METABOLISM-CLINICAL AND EXPERIMENTAL, 2002, 51 (04) :471-476
[6]   Fibrinolysis and diabetic vascular disease: roles of plasminogen activator inhibitor-1 and thrombin-activatable fibrinolysis inhibitor [J].
Aso, Yoshimasa .
FUTURE LIPIDOLOGY, 2006, 1 (04) :429-440
[7]   Comparative effect of angiotensin-converting enzyme inhibition and angiotensin II type 1 receptor antagonism on plasma fibrinolytic balance in humans [J].
Brown, NJ ;
Agirbasli, M ;
Vaughan, DE .
HYPERTENSION, 1999, 34 (02) :285-290
[8]   Synergistic effect of adrenal steroids and angiotensin II on plasminogen activator inhibitor-1 production [J].
Brown, NJ ;
Kim, KS ;
Chen, YQ ;
Blevins, LS ;
Nadeau, JH ;
Meranze, SG ;
Vaughan, DE .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2000, 85 (01) :336-344
[9]   Morphologic findings of coronary atherosclerotic plaques in diabetics - A postmortem study [J].
Burke, AP ;
Kolodgie, FD ;
Zieske, A ;
Fowler, DR ;
Weber, DK ;
Varghese, PJ ;
Farb, A ;
Virmani, R .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2004, 24 (07) :1266-1271
[10]   Induction of hyperinsulinemia combined with hyperglycemia and hypertriglyceridemia increases plasminogen activator inhibitor 1 in blood in normal human subjects [J].
Calles-Escandon, J ;
Mirza, SA ;
Sobel, BE ;
Schneider, DJ .
DIABETES, 1998, 47 (02) :290-293