Abstract
The morphology of human atherosclerotic plaques ranges from a solid fibrous structure to those with substantial lipid cores, covered by only a thin fibrous cap on its luminal aspect [1-4]. Pathological studies have demonstrated that rupture of these coronary atheromas precipitates the formation of the occluding thrombus that causes an acute coronary syndrome, such as unstable angina or myocardial infarction [4]. Plaque-rupture predominantly occurs on the edges of the plaque’s fibrous cap, the shoulder region, areas frequently associated with accumulations of monocyte-derived macrophages, T lymphocytes and mast cells in close proximity to vascular smooth muscle cells [1,4,5]. These activated macrophages and T lymphocytes stimulate their neighboring cells to erode the collagen and elastin, via the release of inflammatory cytokines, resulting in a decay of the framework which forms the plaque’s cap and ultimately leading to the plaque’s rupture [1,5,6].
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References
Ross R.(1993) Pathogenesis of artherosclerosis: a perspective for the 1990s. Nature 362:801–809
Alexander RW.(1994) Inflammation and coronary artery disease. N Engl J Med 331 (7):468–469
Libby P.(1995) Molecular bases of the acute coronary syndrome. Circulation 21:2844–2850
Davies MJ, Thomas AC (1985) Plaque fissuring: the cause of acute myocardial infarc-tion, sudden ischemic death, and crescendo angina.Br Heart J53: 363–373
Van der Waal AC, Becker AE, Loos CM, Das PK (1994) Site of intimai rupture or erosion of thrombosed coronary artherosclerotic plaques is characterized by an inflammatory process irrespective of the dominant plaque morphology.Circulation89: 34–44
Ross R.(1999) Atherosclerosis - an inflammatory disease. N Engl J Med 340 (2): 115–126
Aldermann MH, Madhavan S, Ooi WL, Cohen H, Sealy JE, Laragh JH (1991) Association of the renin-sodium profile with the risk of myocardial infarction in patients with hypertension.N Engl J Med324: 1098–1104
Cambien F, Poirier O, Lecerf L, Evans A, Cambou JP, Arvelier D, Luc G, Bard JM, Bara R, Richard S et al (1992) Deletion polymorphism in the gene for angiotensin-converting enzyme is a potent risk factor for myocardial infarction.Nature359: 641–644
Cambien F, Costerousse O, Tirret L, Poirier O, Lecerf L, Gonzales MF, Evans A, Arveilier D, Cambou JP, Luc G et al (1994) Plasma levels and gene polymorphism of angiotensin converting enzyme in relation to myocardial infarction.Circulation90: 669–676
Ludwig E, Corneli PS, Anderson JL, Marshall HW, Lalouel JM, Ward RL (1995) Angiotensin-converting enzyme gene polymorphism is associated with myocardial infarction but not with development of coronary stenosis. Circulation 91 (8): 2120–2124
Danser AH, Schalekamp MA, Bax WA,van den Brink AM, Saxena PR, Riegger GA, Schunkert H (1995) Angiotensin-converting enzyme in the human heart. Effect of the deletion/insertion polymorphism.Circulation92 (6): 1387–1388
Hernandez-Presa M, Bustos C, Ortega M, Tunon J, Renedo G, Ruiz-Ortega M, Egidio J (1997) Angiotensin-converting enzyme inhibition prevents arterial nuclear factor-KB activation, monocyte chemoattactant proetein-1 expression and macrophage infiltration in a rabbit model of early accelerated atherosclerosis.Circulation95: 1532–1541
Griendling KK, Alexander RW (1997) Oxidative stress and cardiovascular disease.Circulation96: 3264–3265
Griendling KK, Minieri CA, OLLerenshaw JD, Alexander RW (1994) Angiotensin II stimulates NADH and NADPH oxidase activity in cultured vascular smooth muscle cells. Circ Res74 (6): 1141–1148
Chakraborti S, Chakraborti T (1998) Oxidant-mediated activation of mitogen-activated protein kinases and nuclear transcription factors in the cardiovascular system: a brief overview.Cell Signal 10 (10):675–683
Northermann W, Braciak TA, Hattori M, Lee F, Fey GH (1989) Structure of the rat IL-6 gene and its expression in macrophage-derived cells.J Biol Chem264: 16072–16082
Kishimoto T, Akira S, Narazaki M, Taga T (1995) IL-6 family of cytokines and gp130.Blood86: 1243–1254
Fuhrman B, Oiknine J, Aviram M (1994) Iron induces lipid peroxidation in culturedmacrophages, increases their ability to oxidatively modify LDL and affect their secretory properties. Atherosclerosis 111: 65–78
Keidar S, Attias J, Smith J, Breslow JL, Hayek T (1997) The angiotensin II receptor antagonist, losartan, inhibits LDL lipid peroxidation and atherosclerosis in apolipoprotein E deficient mice. Biochem Biophys Res Commun 236: 622–625
Chobanian AV, Haudenschild CC, Nickerson C, Drago R, (1990) Antiartherogenic effect of captopril in Watanabe herritable hyperlipidemic rabbits. Hypertension 15: 327–331
Hayek T, Keidar S, Mei-Yi, Oikine J, Breslow J (1995) Effect of angiotensin converting enzyme inhibitors on LDL lipid peroxidation and artherosclerosis progression in apoE deficient mice. Circulation 92 (Suppl I): I-625
Aberg G, Ferrer P (1990) Effects of Captopril on artherosclerosis in cynomoglus monkeys. J Cardiovasc Pharmacol 15 (Suppl I): S65–S72
Ridker PM, Gaboury CJL, Conlin PR, Seely EW, Williams GH, Vaughan DE (1993) Stimulation of plasminogen activator inhibitor in vivo by infusion of angiotensin II: evidence of a potential interaction between the renin-angiotensin system and fibrinolytic function. Circulation 87: 1969–1973
Ridker PM, Vaughan DE (1995) Hemostatic factors and the risk of myocardial infarction. N Engl J Med 333 (6): 389–390
Pfeffer M, Braunwald E, Moye L, Basta L, Brown EJ, Cuddy TE, Davis BR, Geltmann EM, Goldman S, Fiaker GC et al (1992) Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction: Results of the survival and ventricular enlargement trial. N Engl J Med 327: 669–677
The SOLVD Investigators: (1992) Effect of enalapril on mortality and the development of heart failure in asymptomatic patients with reduced left ventricular ejection fraction. N Engl J Med 327: 568–574
Yusuf N for the investigators of the HOPE Trial (2000) N Engl J Med 342: 145–153
Daemen MJ, Lombardi DM, Bosman FT, Schwartz SM (1991) Angiotensin II induces smooth muscle cell proliferation in the normal and injured rat arterial wall. Circ Res 68: 450–456
Powell JS, Clozel JP, Muller RK, Kuhn H, Hefti F, Hosang M, Baumgartner HR (1989) Inhibitors of angiotensin-converting enzyme prevent myointimal proliferation after vascular injury. Science 245: 186–188
Schieffer B, Paxton WG, Marrero MB, Bernstein KE (1996) Importance of tyrosine phosphorylation in Angiotensin II ATl receptor mediated signalling. Hypertension 27: 476–480
Gibbons GH, Pratt RE, Dzau VJ (1992) Vascular smooth muscle cell hypertrophy versus hyperplasia. Autocrine transforming growth factor-beta 1 expression determines growth response to angiotensin II. J Clin Invest 90 (2): 456–461
Fantl WJ, Johnson DE, Williams LT (1993) Signalling by receptor tyrosine kinases. Annu Rev Biochem 62: 453–481
Sadoshima J, Izumo S (1993) Signal transduction pathways of angiotensin II induced cfos gene expression in cardiac myocytesin vitro. Circ Res73: 424–438
Naftilan AJ, Pratt RE, Dzau VJ (1989) Induction of platelet-derived growth factor A-chain and c-myc gene expression by angiotensin II in cultured rat vascular smooth muscle cells.J Clin Invest83: 1419–1424
Schindler C, Darnell JE (1995) Transcriptional responses to polypeptide ligands: the Jak-Stat pathway.Annu Rev Biochem64: 621–651
Van Der Geer, Hunter T, Lindberg RA (1994) Receptor protein tyrosine kinases and their signal transduction.Annu Rev Cell Biol10: 251–338
Darnell JE, Kerr IM, Stark GR (1994) JAK-Stat pathways and transcriptional activation in response to IFNs and other extracellular signaling proteins.Science264: 1415–1421
Marrero MB, Schieffer B, Paxton WG, Heerdt L, Berk BC, Delafontaine P, Bernstein KE (1995) Direct stimulation of JAK/STAT pathway by the angiotensin II ATlreceptor.Nature375: 247–250
Bhat CJ, Thekkumara TJ, Thomas WG, Conrad KM, Baker KM (1994) Angiotensin II stimulates sis-inducing factor-like DNA binding activity. Evidence that the AT1Areceptor activates transription factor stat9l and/or a related protein.J Biol Chem269: 31443–31449
Biassuci L, Vitelli A, Liuzzo G, Altamura S, Caliguri G, Monaco C, Rebuzzi A, Ciliberto G, Maseri A (1996) Elevated levels of interleukin-6 in unstable angina.Circulation94: 874–877
Marx N, Neumann FJ, Ott I, Gawaz M, Koch W, Pikau T, Schömig A (1997) Induction of cytokine expression in leucocytes in acute myocardial infarction.J Am Coll Cardiol30: 165–170
Solis-Herruzo JA, Rippe A, Schrum LW, de la Torre P, Immaculada G, Jeffrey J, MunozYague T, Brenner D (1996) Interleukin 6 increases metalloproteinases-13 gene expression through stimulation of activator protein 1 transcription factor in cultured fibroblastsJ Biol Chem274 (43): 30919–30926
Diet F, Pratt R, Berry GJ, Momose N, Gibbons G, Dzau VJ (1996) Increased accumulation of tissue ACE in human artherosclerotic coronary artery disease.Circulation94: 2756–2767
Potter DD, Sobey CG, Tompkins PK, Rossen JD, Heistad DD (1998) Evidence that macrophages in atherosclerotic lesions contain angiotensin II.Circulation98: 800–807
Ohishi M, Ueda M, Rakugi H, Naruko T, Kolima A, Okamura A, Higaki J, Ogihara T (1999) Relative localization of angiotensin-converting enzyme, chymase and angiotensin II in human coronary atherosclerotic lesion.J Hypertens17: 547–553
Schieffer B, Schieffer E, Hilfiker-Kleiner D, Hilfiker A, Kovanen P, Nussberger J, Barringer W, Drexler H (2000) Expression of angiotensin II in human coronary atherosclerotic plaques — Potential implications for inflammtation and plaque instability.Circulation101 (12): 1372–1378
Moreno PR, Falk E, Palaivos IF, Newell JB, Fuster V, Fallon JT(1994) Macrophage infiltration in acute coronary syndromes. Implications for plaque rupture.Circulation90: 775–778
Han Y, Runge M, Brasier A (1999) Angiotensin II induces interleukin-6 transcription in vascular smooth muscle cells through pleiotropic activation of nuclear factor-KB transcription factor.Circ Res84: 695–703
Pagano PJ, Clark JK, Cifuentes-Pagano ME, Clark SM, Callis GM, Quinn MT (1997) Localization of a constitutively active, phagocyte-like NADPH oxidase in rabbit aortic adventitia: enhancement by angiotensin II.Proc Natl Acad Sci USA94 (26): 14483–14488
Schieffer B, Kowert A, Brauer N, Wengler A, Schieffer E, Gutzke S, Harringer W, Haverich A, Drexler H (1998) Irbesartan inhibits angiotensin II-induced pro-inflammatory and prothrombotic factors in human coronary arteries: Role of the Jak/STAT cascade.Europ Heart J(Suppl II) P322
Skeggs LT, Dorer FE, Kahn JR, Lentz KE, Levin M (1981) Experimental renal hypertension: The discovery of the renin-angiotensin system. In: RL Soffer (ed):Biochemical regulation of blood pressure.WileyNew York, NY, 3–38
Loree HM, Kamm RD, Stringfellow RG, Lee RT (1992) Effects of fibrous cap thickness on peak circumferential stress in model artherosclerotic vessels.Circ Res71: 850–858
Richardson PD, Davies MJ, Born GV (1989) Influence of plaque configuration and stress distribution on fissuring of coronary atherosclerotic plaques.Lancet21; 2 (8669): 941–944
Schieffer B, Wagner M, Hilfiker-Kleiner D, Hilfiker A, Drexler H (1999) NADPH-oxidase dependent activation of Jak/STAT cascade by angiotensin II: Role of p47phox. Circulation (Suppl II) P-355 (Abstract)
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Schieffer, B., Drexler, H. (2001). Role of Interleukins in Relation to the Renin-Angiotensinsystem in Atherosclerosis. In: Mehta, J.L. (eds) Inflammatory and Infectious Basis of Atherosclerosis. Progress in Inflammation Research. Birkhäuser, Basel. https://doi.org/10.1007/978-3-0348-8239-2_9
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DOI: https://doi.org/10.1007/978-3-0348-8239-2_9
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