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0033752717
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Plasminogen activator inhibitor type 1 is a potential target in renal fibrogenesis
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Rerolle JP, Hertig A, Nguyen G, et al. Plasminogen activator inhibitor type 1 is a potential target in renal fibrogenesis. Kidney Int 2000; 58:1841-1850.
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Rerolle, J.P.1
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0036068351
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Plasminogen activator inhibitor-1 and the kidney
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Eddy A. Plasminogen activator inhibitor-1 and the kidney. Am J Physiol 2002; 283:F209-F220. An extensive and comprehensive review of the potential role of PAI-1 during acute and chronic renal diseases.
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Am J Physiol
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Eddy, A.1
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0034898853
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Enhanced fibrinolytic potential in mice with combined homozygous deficiency of alpha2-antiplasmin and PAI-1
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Dewerchin M, Collen D, Lijnen HR. Enhanced fibrinolytic potential in mice with combined homozygous deficiency of alpha2-antiplasmin and PAI-1. Thromb Haemost 2001; 86:640-646. In this study, the absence of PAI-1 did not influence the amount of fibrin deposited in the kidneys after endotoxin injection, questioning the importance of PAI-1 regarding the surveillance of intra-renal fibrinolysis.
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Thromb Haemost
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Dewerchin, M.1
Collen, D.2
Lijnen, H.R.3
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4
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0038512474
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Plasminogen activator inhibitor-1 is a significant determinant of renal injury in experimental crescentic glomerulonephritis
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Kitching AR, Kong YZ, Huang XR, et al. Plasminogen activator inhibitor-1 is a significant determinant of renal injury in experimental crescentic glomerulonephritis. J Am Soc Nephrol 2003; 14:1487-1495. A study in which the intensity of the fibrin deposits in the glomerular tuft and the infiltration by leukocytes are directly correlated with the PAI-1 gene dosage, suggesting that PAI-1 could play a major, negative role in glomerular fibrinolysis and inflammation.
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J Am Soc Nephrol
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Kitching, A.R.1
Kong, Y.Z.2
Huang, X.R.3
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5
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1642296148
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Type 1 plasminogen activator inhibitor deficiency aggravates the course of experimental glomerulonephritis through TGF-beta overactivation
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Hertig A, Berrou J, Allory Y, et al. Type 1 plasminogen activator inhibitor deficiency aggravates the course of experimental glomerulonephritis through TGF-beta overactivation. FASEB J 2003; 17:1904-1906. In this study, the absence of PAI-1 paradoxically exacerbated the course of passive, anti-GBM glomerulonephritis, and enhanced fibrin deposition, by a mechanism that involved the regulation of the activation of TGF-β by plasminogen activators, independently of plasmin.
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FASEB J
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Hertig, A.1
Berrou, J.2
Allory, Y.3
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Crescentic glomerulonephritis is diminished in fibrinogen-deficient mice
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Drew AF, Tucker HL, Liu H, et al. Crescentic glomerulonephritis is diminished in fibrinogen-deficient mice. Am J Physiol 2001; 281:F1157-F1163.
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Am J Physiol
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Drew, A.F.1
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0035947756
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New tricks for old dogs: Non thrombotic effects of thrombin in vessel wall biology
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Patterson C, Stouffer GA, Madamanchi N, Runge MS. New tricks for old dogs: non thrombotic effects of thrombin in vessel wall biology. Circ Res 2001; 88:987-997.
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Circ Res
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Patterson, C.1
Stouffer, G.A.2
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Runge, M.S.4
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8
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0030954682
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The suicide substrate reaction between plasminogen activator inhibitor 1 and thrombin is regulated by the cofactors vitronectin and heparin
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van Meijer M, Smilde A, Tans G, et al. The suicide substrate reaction between plasminogen activator inhibitor 1 and thrombin is regulated by the cofactors vitronectin and heparin. Blood 1997; 90:1874-1882.
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Van Meijer, M.1
Smilde, A.2
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9
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0035865213
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Blockade of TGF-β signaling in T cells prevents the development of experimental glomerulonephritis
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Kanamaru Y, Nakao A, Mamura M, et al. Blockade of TGF-β signaling in T cells prevents the development of experimental glomerulonephritis. J Immunol 2001; 166:2818-2823.
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J Immunol
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Kanamaru, Y.1
Nakao, A.2
Mamura, M.3
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10
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0037792930
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Blockade of TGF-beta ameliorates renal dysfunction and histologic progression in anti-GBM nephritis
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Zhou A, Ueno H, Shimomura M, et al. Blockade of TGF-beta ameliorates renal dysfunction and histologic progression in anti-GBM nephritis. Kidney Int 2003; 64:92-101. In this study, the systemic blockade of TGF-β by specific gene therapy improved the outcome of anti-GBM nephritis.
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Kidney Int
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, pp. 92-101
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Zhou, A.1
Ueno, H.2
Shimomura, M.3
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11
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0030054203
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Bleomycin-induced pulmonary fibrosis in transgenic mice that either lack or overexpress the murine plasminogen activator inhibitor-1 gene
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Eitzman DT, McCoy RD, Zheng X, et al. Bleomycin-induced pulmonary fibrosis in transgenic mice that either lack or overexpress the murine plasminogen activator inhibitor-1 gene. J Clin Invest 1996; 97:232-237.
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Eitzman, D.T.1
McCoy, R.D.2
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12
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0033659495
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Bleomycin-induced pulmonary fibrosis in fibrinogen-null mice
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Hattori N, Degen JL, Sisson TH, et al. Bleomycin-induced pulmonary fibrosis in fibrinogen-null mice. J Clin Invest 2000; 106:1341-1350.
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J Clin Invest
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Hattori, N.1
Degen, J.L.2
Sisson, T.H.3
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13
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0035859783
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Plasminogen activator inhibitor-1 deficiency prevents hypertension and vascular fibrosis in response to long-term nitric oxide synthase inhibition
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Kaikita K, Fogo AB, Ma L, et al. Plasminogen activator inhibitor-1 deficiency prevents hypertension and vascular fibrosis in response to long-term nitric oxide synthase inhibition. Circulation 2001; 104:839-844.
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Circulation
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Kaikita, K.1
Fogo, A.B.2
Ma, L.3
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14
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0034912450
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PAI-1 deficiency attenuates the fibrogenic response to ureteral obstruction
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Oda T, Jung YO, Kim HS, et al. PAI-1 deficiency attenuates the fibrogenic response to ureteral obstruction. Kidney Int 2001; 60:587-596.
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Kidney Int
, vol.60
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Oda, T.1
Jung, Y.O.2
Kim, H.S.3
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15
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0042388115
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A mutant, noninhibitory plasminogen activator inhibitor type 1 decreases matrix accumulation in experimental glomerulonephritis
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Huang Y, Haraguchi M, Lawrence DA, et al. A mutant, noninhibitory plasminogen activator inhibitor type 1 decreases matrix accumulation in experimental glomerulonephritis. J Clin Invest 2003; 112:379-388. The first study to demonstrate that therapeutic intervention with PAI-1 inhibitors may reduce glomerular fibrosis, by competing with endogenous PAI-1.
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J Clin Invest
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, pp. 379-388
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Huang, Y.1
Haraguchi, M.2
Lawrence, D.A.3
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16
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0345249708
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Endogenous plasmin is not protective in unilateral ureteric ligation induced renal interstitial fibrosis
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Edgtton KL, Carmeliet P, Kitching AR. Endogenous plasmin is not protective in unilateral ureteric ligation induced renal interstitial fibrosis [Abstract]. Am Soc Nephrol 2002; 13:539A.
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Am Soc Nephrol
, vol.13
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Edgtton, K.L.1
Carmeliet, P.2
Kitching, A.R.3
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17
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0042134798
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Plasminogen activator inhibitor-1 supports IL-8-mediated transendothelial migration by inhibition of the constitutive shedding of endothelial IL-8/heparan sulfate/syndecan-1 complexes
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Marshall LJ, Ramdin LS, Brooks T, et al. Plasminogen activator inhibitor-1 supports IL-8-mediated transendothelial migration by inhibition of the constitutive shedding of endothelial IL-8/heparan sulfate/syndecan-1 complexes. J Immunol 2003; 171:2057-2065. In an original approach, the authors report that PAI-1 is involved in the stabilization of a mediator of inflammation, by a plasmin-dependent mechanism.
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J Immunol
, vol.171
, pp. 2057-2065
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Marshall, L.J.1
Ramdin, L.S.2
Brooks, T.3
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18
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0036854980
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Disruption of tissue-type plasminogen activator gene in mice reduces renal interstitial fibrosis in obstructive nephropathy
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Yang J, Shultz RW, Mars WM, et al. Disruption of tissue-type plasminogen activator gene in mice reduces renal interstitial fibrosis in obstructive nephropathy. J Clin Invest 2002; 110:1525-1538. Unexpectedly, the absence of tPA is shown to play a protective role during UUO. Originally, the authors demonstrated that tPA induces matrix metalloproteinase 9 gene expression by renal interstitial fibroblasts, and promotes epithelial-to-myofibroblast transition.
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J Clin Invest
, vol.110
, pp. 1525-1538
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Yang, J.1
Shultz, R.W.2
Mars, W.M.3
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19
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0037407704
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Urokinase receptor deficiency accelerates renal fibrosis in obstructive nephropathy
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Zhang G, Kim HS, Cai X, et al. Urokinase receptor deficiency accelerates renal fibrosis in obstructive nephropathy. J Am Soc Nephrol 2003; 14:1254-1271. uPAR is shown to lower renal fibrosis in the UUO model, by a mechanism that could involve the activation of hepatocyte growth factor by uPA.
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J Am Soc Nephrol
, vol.14
, pp. 1254-1271
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Zhang, G.1
Kim, H.S.2
Cai, X.3
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21
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0030685740
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Inhibitory role of plasminogen activator inhibitor-1 in arterial wound healing and neointima formation
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Carmeliet P, Moons L, Lijnen HR, et al. Inhibitory role of plasminogen activator inhibitor-1 in arterial wound healing and neointima formation. Circulation 1997; 96:3180-3191.
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Circulation
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Carmeliet, P.1
Moons, L.2
Lijnen, H.R.3
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22
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0035899858
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Plasminogen activator inhibitor-1 increases neointima formation in balloon-injured rat carotid arteries
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DeYoung MB, Tom C, Dichek DA. Plasminogen activator inhibitor-1 increases neointima formation in balloon-injured rat carotid arteries. Circulation 2001; 104:1972-1981.
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Circulation
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DeYoung, M.B.1
Tom, C.2
Dichek, D.A.3
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23
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0033580594
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Increased plasminogen activator inhibitor-1 and vasculopathy: A reconcilable paradox
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Sobel B. Increased plasminogen activator inhibitor-1 and vasculopathy: a reconcilable paradox. Circulation 1999; 99:2496-2498. An elegant discussion, in which the author discusses the contradictory findings reported on the impact of PAI-1 expression in vivo during atherosclerotic disease.
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(1999)
Circulation
, vol.99
, pp. 2496-2498
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Sobel, B.1
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24
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0034518414
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PAI-1, fibrosis, and the elusive provisional fibrin matrix
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Loskutoff DJ, Quigley JP. PAI-1, fibrosis, and the elusive provisional fibrin matrix. J Clin Invest 2000; 106:1441-1443.
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(2000)
J Clin Invest
, vol.106
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Loskutoff, D.J.1
Quigley, J.P.2
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25
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0032030912
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Fibrinogen deficiency is compatible with the development of atherosclerosis in mice
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Xiao Q, Danton MJ, Witte DP, et al. Fibrinogen deficiency is compatible with the development of atherosclerosis in mice. J Clin Invest 1998; 101:1184-1194.
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J Clin Invest
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Xiao, Q.1
Danton, M.J.2
Witte, D.P.3
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26
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0342545947
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Atherosclerosis progression in LDL receptor-deficient and apolipoprotein E-deficient mice is independent of genetic alterations in plasminogen activator inhibitor-1
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Sjöland H, Eitzman DT, Gordon D, et al. Atherosclerosis progression in LDL receptor-deficient and apolipoprotein E-deficient mice is independent of genetic alterations in plasminogen activator inhibitor-1. Arterioscler Thromb Vasc Biol 2000; 20:846-852.
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Arterioscler Thromb Vasc Biol
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Sjöland, H.1
Eitzman, D.T.2
Gordon, D.3
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27
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0036124715
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Lack of plasminogen activator inhibitor-1 promotes growth and abnormal matrix remodeling of advanced atherosclerotic plaques in apolipoprotein E-deficient mice
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Luttun A, Lupu F, Storkebaum E, et al. Lack of plasminogen activator inhibitor-1 promotes growth and abnormal matrix remodeling of advanced atherosclerotic plaques in apolipoprotein E-deficient mice. Arterioscler Thromb Vasc Biol 2002; 22:499-505. The paradoxically protective role of PAI-1 is reported in a model of accelerated vascular fibrosis. The absence of PAI-1 results in the deposition of a chaotic matrix and in the overactivation of TGF-β (this is the first demonstration in vivo).
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(2002)
Arterioscler Thromb Vasc Biol
, vol.22
, pp. 499-505
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Luttun, A.1
Lupu, F.2
Storkebaum, E.3
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28
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0034672348
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Plasminogen activator inhibitor-1 deficiency protects against atherosclerosis progression in the mouse carotid artery
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Eitzman DT, Westrick RJ, Xu Z, et al. Plasminogen activator inhibitor-1 deficiency protects against atherosclerosis progression in the mouse carotid artery. Blood 2000; 96:4212-4215.
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Blood
, vol.96
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Eitzman, D.T.1
Westrick, R.J.2
Xu, Z.3
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29
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0037162388
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Age-dependent spontaneous coronary arterial thrombosis in transgenic mice that express a stable form of human plasminogen activator inhibitor-1
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Eren M, Painter CA, Atkinson JB, et al. Age-dependent spontaneous coronary arterial thrombosis in transgenic mice that express a stable form of human plasminogen activator inhibitor-1. Circulation 2002; 106:491-496. A key study, demonstrating that PAI-1 is critically involved in the pathogenesis of coronary atherosclerosis, and in which PAI-1-overexpressing mice die of myocardial stroke.
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(2002)
Circulation
, vol.106
, pp. 491-496
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Eren, M.1
Painter, C.A.2
Atkinson, J.B.3
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