The Link Between Vascular Features and Thrombosis

被引:69
作者
Esmon, Charles T. [1 ,2 ,3 ,4 ]
Esmon, Naomi L. [1 ]
机构
[1] Oklahoma Med Res Fdn, Cardiovasc Biol Res Program, Oklahoma City, OK 73104 USA
[2] Univ Oklahoma, Hlth Sci Ctr, Howard Hughes Med Inst, Oklahoma City, OK 73104 USA
[3] Univ Oklahoma, Hlth Sci Ctr, Dept Pathol, Oklahoma City, OK 73104 USA
[4] Univ Oklahoma, Hlth Sci Ctr, Dept Biochem & Mol Biol, Oklahoma City, OK 73104 USA
来源
ANNUAL REVIEW OF PHYSIOLOGY, VOL 73 | 2011年 / 73卷
关键词
endothelium; thrombomodulin; thrombin; antithrombin; microvasculature; ACTIVATED PROTEIN-C; TUMOR-NECROSIS-FACTOR; FACTOR PATHWAY INHIBITOR; HUMAN ENDOTHELIAL-CELLS; DEEP-VEIN THROMBOSIS; FACTOR-V-LEIDEN; TISSUE FACTOR; VENOUS THROMBOSIS; BLOOD-COAGULATION; THROMBOMODULIN COMPLEX;
D O I
10.1146/annurev-physiol-012110-142300
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
The mechanisms of vascular control of thrombotic events remain unclear. The vasculanire possesses essential anticoagulant factors that regulate coagulation. Because the endothelium-to-blood ratios are much higher in the microcirculation, it is likely that stasis contributes to thrombotic risk, due in large part to failure to rapidly access the microcirculation and to gain access to this highly anticoagulant environment. Inflammation can potentiate thrombosis in part through down-regulation of the vascular anticoagulants, a process that appears to be exacerbated in aging, a well-known risk factor for thrombosis. Surgery and trauma, two major risk factors for thrombosis, result in the release of a variety of cellular components that trigger coagulation through separate mechanisms.
引用
收藏
页码:503 / 514
页数:12
相关论文
共 82 条
[1]   The N-terminal domain of thrombomodulin sequesters high-mobility group-B1 protein, a novel antiinflammatory mechanism [J].
Abeyama, K ;
Stern, DM ;
Ito, Y ;
Kawahara, K ;
Yoshimoto, Y ;
Tanaka, M ;
Uchimura, T ;
Ida, N ;
Yamazaki, Y ;
Yamada, S ;
Yamamoto, Y ;
Yamamoto, H ;
Iino, S ;
Taniguchi, N ;
Maruyama, I .
JOURNAL OF CLINICAL INVESTIGATION, 2005, 115 (05) :1267-1274
[2]   TAFI, or plasma procarboxypeptidase B, couples the coagulation and fibrinolytic cascades through the thrombin-thrombomodulin complex [J].
Bajzar, L ;
Morser, J ;
Nesheim, M .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1996, 271 (28) :16603-16608
[3]  
Bertina RM, 1997, CLIN CHEM, V43, P1678
[4]  
BRANSON HE, 1983, LANCET, V2, P1165
[5]   REGULATION OF COAGULATION BY A MULTIVALENT KUNITZ-TYPE INHIBITOR [J].
BROZE, GJ ;
GIRARD, TJ ;
NOVOTNY, WF .
BIOCHEMISTRY, 1990, 29 (33) :7539-7546
[6]   Factor Xa is highly protected from antithrombin-fondaparinux and antithrombin-enoxaparin when incorporated into the prothrombinase complex [J].
Brufatto, N ;
Ward, A ;
Nesheim, ME .
JOURNAL OF THROMBOSIS AND HAEMOSTASIS, 2003, 1 (06) :1258-1263
[7]  
BUSCH C, 1982, LAB INVEST, V47, P498
[8]   Inactivation of C3a and C5a octapeptides by carboxypeptidase R and carboxypeptidase N [J].
Campbell, WD ;
Lazoura, E ;
Okada, N ;
Okada, H .
MICROBIOLOGY AND IMMUNOLOGY, 2002, 46 (02) :131-134
[9]   ACTIVATION OF PROTEIN-C INVIVO [J].
COMP, PC ;
JACOCKS, RM ;
FERRELL, GL ;
ESMON, CT .
JOURNAL OF CLINICAL INVESTIGATION, 1982, 70 (01) :127-134
[10]   Thrombin signalling and protease-activated receptors [J].
Coughlin, SR .
NATURE, 2000, 407 (6801) :258-264