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[1]Schonbeck U, Libby P. CD40 signaling and plaque instability[J]. Circ Res, 2001, 89(12):1092-1103.
[2]Nagashima H, Aoka Y, Sakomura Y, et al. Matrix metalloproteinase 2 is suppressed by trapidil, a CD40-CD40 ligand pathway inhibitor, in human abdominal aortic aneurysm wall[J]. J Vasc Surg, 2004, 39(2):447-453.
[3]Smola-Hess S, Schnitzler R, Hadaschik D, et al. CD40L induces matrix-metalloproteinase-9 but not tissue inhibitor of metalloproteinases-1 in cervical carcinoma cells: imbalance between NF-kappaB and STAT3 activation[J]. Exp Cell Res, 2001, 267(2):205-215.
[4]Santovito D, Mezzetti A, Cipollone F. Cyclooxygenase and prostaglandin synthases: roles in plaque stability and instability in humans[J]. Curr Opin Lipidol, 2009, 20(5):402-408.
[5]Bujold K, Rhainds D, Jossart C, et al. CD36-mediated cholesterol efflux is associated with PPARgamma activation via a MAPK-dependent COX-2 pathway in macrophages[J]. Cardiovasc Res, 2009, 83(3):457-464.
[6]Rival Y, Puech L, Taillandier T, et al. PPAR activators and COX inhibitors selectively block cytokine-induced COX-2 expression and activity in human aortic smooth muscle cells[J]. Eur J Pharmacol, 2009, 606(1-3):121-129.
[7]Rupp J, Berger M, Reiling N, et al. Cox-2 inhibition abrogates Chlamydia pneumoniae-induced PGE2 and MMP-1 expression[J]. Biochem Biophys Res Commun, 2004, 320(3):738-744.
[8]Choi YA, Lee DJ, Lim HK, et al. Interleukin-1beta stimulates matrix metalloproteinase-2 expression via a prostaglandin E2-dependent mechanism in human chondrocytes[J]. Exp Mol Med, 2004, 36(3):226-232.
[9]Cipollone F, Fazia M, Iezzi A, et al. Blockade of the angiotensin II type 1 receptor stabilizes atherosclerotic plaques in humans by inhibiting prostaglandin E2-dependent matrix metalloproteinase activity[J]. Circulation, 2004, 109(12):1482-1488.
[10]Pillinger MH, Rosenthal PB, Tolani SN, et al. Cyclooxygenase-2-derived E prostaglandins down-regulate matrix metalloproteinase-1 expression in fibroblast-like synoviocytes via inhibition of extracellular signal-regulated kinase activation[J]. J Immunol, 2003, 171(11):6080-6089.