1[1]Galis ZS,Sukhova GK,Lark MW,et al.Increased expression of matrix metalloproteinases and matrix degrading activity in vulnerable regions of human atherosclerotic plaque s[J].J Clin Invest,1994,94:2493-2503.
2[2]Galis ZS,Johnson C,Godin D,et al.Targeted disruption of the matrix metalloproteinase-9 gene impairs smooth muscle cell migration and geometrical arterial remodeling[J].Circ Res,2002,91:852-859.
3[3]Galis ZS,Khatri JJ.Matrix metalloproteinase in vascular remodeling and atherogenesis:the good,the bad,and the ugly[J].Circ Res,2002,90:251-262.
9[9]Vesey DA,Cheung CW,Kruger WA,et al.Thrombin stimulates Proinflammatory and proljferative responses in primary cultures of human proximal tubule cells[J].Kidney Int,2005,67:1315-1329.
10[10]Shaw PX,Horkko S,Tsireikas S,et al.Human-derived anti-oxidized LDL autoantibodv blocks uptake of oxidized LDL by macrophages and localizes to atherosclerotic lesions in vivor[J].Arterioscler Thromb Vasc Biol.2001.21:1254-1255.
4[1]Ambrose JA, Martinez EE. A new paradigm for plaque stabilization. Circulation, 2002, 105 (16): 2 000-004
5[2]Brasen JH, Harsch M, Niendorf A. Survival and cardiovascular pathology of hetero-zygous watanabe heritable hyperlipidaemic rabbits treated with pravastatin and probucol on a low-cholesterol(0.03%)-enriched diet. Virchows Arch, 1998, 432 (6): 557-562
6[3]Brasen JH, Harsch M, Niendorf A. Probucol inhibits not only the progression of atherosclerotic disease, but causes a different composition of atherosclerotic lesions in WHHL-rabbits. Virchows Arch, 1995, 426 (2):179-188
7[4]Xu XP, Meisel SR, Ong JM. Oxidized low-density lipoprotein regulates matrix metalloproteinase-9 and its tissue inhibitor in human moncyte-derived macrophages. Circulation, 1999, 99: 993-998
8[6]Crisby M, Nordin-Fredriksson G, Shah PK. Pravastatin treatment increases collagen content and decreases lipid content, inflammation,metalloproteinases, and cell death in human carotid plaques: implications for plaque stabilization. Circulation, 2001, 103: 926-933
9[7]Libby P. What have we learned about the biology of atherosclerosis? The role of inflammation. Am J Cardiol, 2001, 88: 3J-6J
10[8]Loftus IM, Naylor AR, Goodall S. Increased matrix metalloproteinase-9 activity in unstable carotid plaques. A potential role in acute plaque disruption. Stroke, 2000, 31 (1): 40-47
