Plasminogen activator inhibitor type 1: the two faces of the same coin

被引:25
作者
Hertig, A
Rondeau, E
机构
[1] INSERM, U489, F-75020 Paris, France
[2] Hop Tenon, Dept Nephrol, F-75970 Paris, France
关键词
atherosclerosis; plasmin; plasminogen activator inhibitor 1; transforming growth factor beta;
D O I
10.1097/00041552-200401000-00006
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 [临床医学]; 100201 [内科学];
摘要
Purpose of review Plasminogen activator inhibitor type 1 is the primary inhibitor of plasminogen activators. It is often bound to vitronectin, an abundant component of extracellular matrix in many tissues. The aim of this review is to discuss the contradictory results reported concerning the impact of plasminogen activator inhibitor type 1 expression in the kidney and in the vessel wall during pathological conditions. Recent findings First described as a 'bad guy' promoting the persistence of fibrin deposition and the evolution towards organ fibrosis, plasminogen activator inhibitor type 1 was recently reported to serve an unexpected protective role during fibrin-dependent diseases, such as experimental glomerulonephritis, and during aortic atherosclerosis. Summary Plasminogen activator inhibitor type 1 is not only an inhibitor of plasmin generation. Recent data suggest that plasminogen activator inhibitor type 1 is required for the regulation of plasminogen activator-dependent, plasmin-independent processes, and that its expression in vivo critically modulates inflammation, potentially by its capacity to occupy vitronectin binding sites.
引用
收藏
页码:39 / 44
页数:6
相关论文
共 29 条
[1]
Inhibitory role of plasminogen activator inhibitor-1 in arterial wound healing and neointima formation - A gene targeting and gene transfer study in mice [J].
Carmeliet, P ;
Moons, L ;
Lijnen, HR ;
Janssens, S ;
Lupu, F ;
Collen, D ;
Gerard, RD .
CIRCULATION, 1997, 96 (09) :3180-3191
[2]
Dewerchin M, 2001, THROMB HAEMOSTASIS, V86, P640
[3]
Plasminogen activator inhibitor type I increases neointima formation in balloon-injured rat carotid arteries [J].
DeYoung, MB ;
Tom, C ;
Dichek, DA .
CIRCULATION, 2001, 104 (16) :1972-1977
[4]
Crescentic glomerulonephritis is diminished in fibrinogen-deficient mice [J].
Drew, AF ;
Tucker, HL ;
Liu, H ;
Witte, DP ;
Degen, JL ;
Tipping, PG .
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY, 2001, 281 (06) :F1157-F1163
[5]
Plasminogen activator inhibitor-1 and the kidney [J].
Eddy, AA .
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY, 2002, 283 (02) :F209-F220
[6]
Edgtton KL, 2002, J AM SOC NEPHROL, V13, p539A
[7]
Eitzman DT, 2000, BLOOD, V96, P4212
[8]
Bleomycin-induced pulmonary fibrosis in transgenic mice that either lack or overexpress the murine plasminogen activator inhibitor-1 gene [J].
Eitzman, DT ;
McCoy, RD ;
Zheng, XX ;
Fay, WP ;
Shen, TL ;
Ginsburg, D ;
Simon, RH .
JOURNAL OF CLINICAL INVESTIGATION, 1996, 97 (01) :232-237
[9]
Age-dependent spontaneous coronary arterial thrombosis in transgenic mice that express a stable form of human plasminogen activator inhibitor-1 [J].
Eren, M ;
Painter, CA ;
Atkinson, JB ;
Declerck, PJ ;
Vaughan, DE .
CIRCULATION, 2002, 106 (04) :491-496
[10]
Renal fibrosis: not just PAI-1 in the sky [J].
Fogo, AB .
JOURNAL OF CLINICAL INVESTIGATION, 2003, 112 (03) :326-328