New findings on venous thrombogenesis

被引:51
作者
Byrnes, James R.
Wolberg, Alisa S. [1 ]
机构
[1] Univ N Carolina, Dept Pathol & Lab Med, 819 Brinkhous Bullitt Bldg,CB 7525, Chapel Hill, NC 27599 USA
来源
HAMOSTASEOLOGIE | 2017年 / 37卷 / 01期
基金
美国国家卫生研究院; 美国国家科学基金会;
关键词
Tissue factor; factor XII; antithrombotic; thrombosis models; DEEP-VEIN THROMBOSIS; KRUPPEL-LIKE FACTOR-2; ACTIVATED PROTEIN-C; TISSUE FACTOR EXPRESSION; ELEVATED FACTOR-VIII; CHAIN CROSS-LINKING; FACTOR-XIII; P-SELECTIN; BLOOD-COAGULATION; PROTHROMBIN ACTIVATION;
D O I
10.5482/HAMO-16-09-0034
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Venous thrombosis (VT) is the third most common cause of cardiovascular death worldwide. Complications from VT and pulmonary embolism are the leading cause of lost disability-adjusted life years. Risks include genetic (e.g., non-0 blood group, activated protein C resistance, hyperprothrombinemia) and acquired (e.g., age, surgery, cancer, pregnancy, immobilisation, female hormone use) factors. Pathophysiologic mechanisms that promote VT are incompletely understood, but involve abnormalities in blood coagulability, vessel function, and flow (so-called Virchow's Triad). Epidemiologic studies of humans, animal models, and biochemical and biophysical investigations have revealed contributions from extrinsic, intrinsic, and common pathways of coagulation, endothelial cells, leukocytes, red blood cells, platelets, cell-derived microvesicles, stasis-induced changes in vascular cells, and blood rheology. Knowledge of these mechanisms may yield new therapeutic targets. Characterisation of mechanisms that mediate VT formation and stability, particularly in aging, are needed to advance understanding of VT.
引用
收藏
页码:25 / 35
页数:11
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