Inflammation in atherosclerosis - Nature
- ️Libby, Peter
- ️Thu Dec 19 2002
Murray, C. J. & Lopez, A. D. Global mortality, disability, and the contribution of risk factors: Global Burden of Disease Study. Lancet 349, 1436–1442 (1997).
Ross, R. & Harker, L. Hyperlipidemia and atherosclerosis. Science 193, 1094–1100 (1976).
Libby, P., Ridker, P. M. & Maseri, A. Inflammation and atherosclerosis. Circulation 105, 1135–1143 (2002).
Poole, J. C. F. & Florey, H. W. Changes in the endothelium of the aorta and the behavior of macrophages in experimental atheroma of rabbits. J. Pathol. Bacteriol. 75, 245–253 (1958).
Cybulsky, M. I. & Gimbrone M. A. Jr Endothelial expression of a mononuclear leukocyte adhesion molecule during atherogenesis. Science 251, 788–791 (1991).
Li, H., Cybulsky, M. I., Gimbrone, M. A. Jr & Libby, P. An atherogenic diet rapidly induces VCAM-1, a cytokine regulatable mononuclear leukocyte adhesion molecule, in rabbit endothelium. Arterioscler. Thromb. 13, 197–204 (1993).
Cybulsky, M. I. et al. A major role for VCAM-1, but not ICAM-1, in early atherosclerosis. J. Clin. Invest. 107, 1255–1262 (2001).
Johnson, R. C. et al. Absence of P-selectin delays fatty streak formation in mice. J. Clin. Invest. 99, 1037–1043 (1997).
Dong, Z. M. et al. The combined role of P- and E-selectins in atherosclerosis. J. Clin. Invest. 102, 145–152 (1998).
Collins, T. & Cybulsky, M. I. NF-κB: pivotal mediator or innocent bystander in atherogenesis? J. Clin. Invest. 107, 255–264 (2001).
Topper, J. N. & Gimbrone, M. A. Jr Blood flow and vascular gene expression: fluid shear stress as a modulator of endothelial phenotype. Mol. Med. Today 5, 40–46 (1999).
De Caterina, R. et al. Nitric oxide decreases cytokine-induced endothelial activation. Nitric oxide selectively reduces endothelial expression of adhesion molecules and proinflammatory cytokines. J. Clin. Invest. 96, 60–68 (1995).
Gu, L. et al. Absence of monocyte chemoattractant protein-1 reduces atherosclerosis in low-density lipoprotein-deficient mice. Mol. Cell 2, 275–281 (1998).
Boring, L., Gosling, J., Cleary, M. & Charo, I. F. Decreased lesion formation in CCR2−/− mice reveals a role for chemokines in the initiation of atherosclerosis. Nature 394, 894–897 (1998).
Boisvert, W. A., Santiago, R., Curtiss, L. K. & Terkeltaub, R. A. A leukocyte homologue of the IL-8 receptor CXCR-2 mediates the accumulation of macrophages in atherosclerotic lesions of LDL receptor-deficient mice. J. Clin. Invest. 101, 353–363 (1998).
Mach, F. et al. Differential expression of three T lymphocyte-activating CXC chemokines by human atheroma-associated cells. J. Clin. Invest. 104, 1041–1050 (1999).
Haley, K. J. et al. Overexpression of eotaxin and the CCR3 receptor in human atherosclerosis : using genomic technology to identify a potential novel pathway of vascular. Circulation 102, 2185–2189 (2000).
Clinton, S., Underwood, R., Sherman, M., Kufe, D. & Libby, P. Macrophage-colony stimulating factor gene expression in vascular cells and in experimental and human atherosclerosis. Am. J. Pathol. 140, 301–316 (1992).
Rosenfeld, M. et al. Macrophage colony-stimulating factor mRNA and protein in atherosclerotic lesions of rabbits and humans. Am. J. Pathol. 140, 291–300 (1992).
Smith, J. D. et al. Decreased atherosclerosis in mice deficient in both macrophage colony-stimulating factor (op) and apolipoprotein E. Proc. Natl Acad. Sci. USA 92, 8264–8268 (1995).
Rajavashisth, T. et al. Heterozygous osteopetrotic (op) mutation reduces atherosclerosis in LDL receptor-deficient mice. J. Clin. Invest. 101, 2702–2710 (1998).
Qiao, J. H. et al. Role of macrophage colony-stimulating factor in atherosclerosis: studies of osteopetrotic mice. Am. J. Pathol. 150, 1687–1699 (1997).
Sugiyama, S. et al. Macrophage myeloperoxidase regulation by granulocyte macrophage colony-stimulating factor in human atherosclerosis and implications in acute coronary syndromes. Am. J. Pathol. 158, 879–891 (2001).
Bruschke, A. V. et al. The dynamics of progression of coronary atherosclerosis studied in 168 medically treated patients who underwent coronary arteriography three times. Am. Heart J. 117, 296–305 (1989).
Yokoya, K. et al. Process of progression of coronary artery lesions from mild or moderate stenosis to moderate or severe stenosis: a study based on four serial coronary arteriograms per year. Circulation 100, 903–909 (1999).
Davies, M. J. Stability and instability: the two faces of coronary atherosclerosis. The Paul Dudley White Lecture, 1995. Circulation 94, 2013–2020 (1996).
Virmani, R., Burke, A. P., Farb, A. & Kolodgie, F. D. Pathology of the unstable plaque. Prog. Cardiovasc. Dis. 44, 349–356 (2002).
Faggiotto, A., Ross, R. & Harker, L. Studies of hypercholesterolemia in the nonhuman primate. I. Changes that lead to fatty streak formation. Arteriosclerosis 4, 323–340 (1984).
de Boer, O. J., van der Wal, A. C., Teeling, P. & Becker, A. E. Leucocyte recruitment in rupture prone regions of lipid-rich plaques: a prominent role for neovascularization? Cardiovasc. Res. 41, 443–449 (1999).
Rajavashisth, T. B. et al. Inflammatory cytokines and oxidized low density lipoproteins increase endothelial cell expression of membrane type 1-matrix metalloproteinase. J. Biol. Chem. 274, 11924–11929 (1999).
Brogi, E. et al. Distinct patterns of expression of fibroblast growth factors and their receptors in human atheroma and non-atherosclerotic arteries: association of acidic FGF with plaque microvessels and macrophages. J. Clin. Invest. 92, 2408–2418 (1993).
Ramos, M. A. et al. Induction of macrophage VEGF in response to oxidized LDL and VEGF accumulation in human atherosclerotic lesions. Arterioscler. Thromb. Vasc. Biol. 18, 1188–1196 (1998).
Moulton, K. S. et al. Angiogenesis inhibitors endostatin or TNP-470 reduce intimal neovascularization and plaque growth in apolipoprotein E-deficient mice. Circulation 99, 1726–1732 (1999).
Libby, P. The molecular bases of the acute coronary syndromes. Circulation 91, 2844–2850 (1995).
Lee, R. & Libby, P. The unstable atheroma. Arterioscler. Thromb. Vasc. Biol. 17, 1859–1867 (1997).
Galis, Z., Sukhova, G., Lark, M. & Libby, P. Increased expression of matrix metalloproteinases and matrix degrading activity in vulnerable regions of human atherosclerotic plaques. J. Clin. Invest. 94, 2493–2503 (1994).
Sukhova, G. K. et al. Evidence for increased collagenolysis by interstitial collagenases-1 and -3 in vulnerable human atheromatous plaques. Circulation 99, 2503–2509 (1999).
Herman, M. P. et al. Expression of neutrophil collagenase (matrix metalloproteinase-8) in human atheroma: a novel collagenolytic pathway suggested by transcriptional profiling. Circulation 104, 1899–1904 (2001).
Saren, P., Welgus, H. G. & Kovanen, P. T. TNF-α and IL-1β selectively induce expression of 92-kDa gelatinase by human macrophages. J. Immunol. 157, 4159–4165 (1996).
Kovanen, P. T., Kaartinen, M. & Paavonen, T. Infiltrates of activated mast cells at the site of coronary atheromatous erosion or rupture in myocardial infarction. Circulation 92, 1084–1088 (1995).
Navab, M. et al. High density associated enzymes: their role in vascular biology. Curr. Opin. Lipidol. 9, 449–456 (1998).
Schmidt, A. M., Yan, S. D., Wautier, J. L. & Stern, D. Activation of receptor for advanced glycation end products: a mechanism for chronic vascular dysfunction in diabetic vasculopathy and atherosclerosis. Circ. Res. 84, 489–497 (1999).
Aikawa, M. et al. An HMG-CoA reductase inhibitor, cerivastatin, suppresses growth of macrophages expressing matrix metalloproteinases and tissue factor in vivo and in vitro. Circulation 103, 276–283 (2001).
Ridker, P. M. et al. Inflammation, pravastatin, and the risk of coronary events after myocardial infarction in patients with average cholesterol levels. Cholesterol and Recurrent Events (CARE) Investigators. Circulation 98, 839–844 (1998).
Yusuf, S. et al. Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients. The Heart Outcomes Prevention Evaluation Study Investigators. N. Engl. J. Med. 342, 145–153 (2000).
Dahlof, B. et al. Cardiovascular morbidity and mortality in the Losartan Intervention For Endpoint reduction in hypertension study (LIFE): a randomised trial against atenolol. Lancet 359, 995–1003 (2002).
Libby, P. Current concepts of the pathogenesis of the acute coronary syndromes. Circulation 104, 365–372 (2001).
Marx, N., Sukhova, G. K., Collins, T., Libby, P. & Plutzky, J. PPARα activators inhibit cytokine-induced vascular cell adhesion molecule-1 expression in human endothelial cells. Circulation 99, 3125–3131 (1999).
Marx, N. et al. PPARα activators inhibit tissue factor expression and activity in human monocytes. Circulation 103, 213–219 (2001).
Neve, B. P. et al. PPARα agonists inhibit tissue factor expression in human monocytes and macrophages. Circulation 103, 207–212 (2001).
Delerive, P. et al. Peroxisome proliferator-activated receptor α negatively regulates the vascular inflammatory gene response by negative cross-talk with transcription factors NF-κB and AP-1. J. Biol. Chem. 274, 32048–32054 (1999).