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Vol. 44. Núm. 2.
Páginas 56-63 (enero 2001)
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Vol. 44. Núm. 2.
Páginas 56-63 (enero 2001)
Acceso a texto completo
Impacto del metabolismo lipídico en la aterogénesis femenina
Impact of lipid metabolism in atherogenesis in women
Visitas
3394
M.C. García-Martínez, A. Cano
Autor para correspondencia
antonio.cano@uv.es

Correspondencia: Departamento de Pediatría, Obstetricia y Ginecología. Facultad de Medicina y Odontología. Avda. Blasco Ibáñez, 17. 46010 Valencia
Departamento de Pediatría, Obstetricia y Ginecología. Facultad de Medicina y Odontología. Universidad de Valencia
C. Hermenegildo*
* Unidad Mixta de Investigación. Hospital Clínico Universitario de Valencia
Este artículo ha recibido
Información del artículo
Resumen
Objetivo

Revisar los mecanismos que, ligados al metabolismo lipídico, determinan riesgo vascular en la mujer posmenopáusica

Fuentes

Bibliografía médica hasta septiembre del año 2000 a través de MEDLINE

Conclusiones

Nuevos datos, ligados a la modificación de partículas por oxidación o cambios en su tamaño, aclaran considerablemente la influencia de los lípidos en los procesos de aterogénesis

Palabras clave:
Aterogénesis
Hormonas
Lipoproteínas
Triglicéridos
Menopausia
Impact of lipid metabolism in atherogenesis in women
Aim

To review the mechanisms by which lipid metabolism is linked to cardiovascular risk in postmenopausal women

Data sources

Medical literatura to September 2000, reviewed through Medline

Conclusions

New data on particle modification by oxidation and changes in their size, further explain the role of lipids in atherogenesis

Keywords:
Atherogenesis
Hormones
Lipoproteins
Triglycerides
Menopause
El Texto completo está disponible en PDF
Bibliografía
[1.]
T.L. Bush.
The epidemiology of cardiovascular disease in postmenopausal women.
Ann N Y Acad Sci, 592 (1990), pp. 263-271
[2.]
W.P. Castelli.
Epidemiology of coronary heart diseases: the Framingham study.
Am J Med, 76 (1984), pp. 4-12
[3.]
R. Ross.
Cell biology of atherosclerosis.
Annu Rev Physiol, 57 (1995), pp. 791-804
[4.]
G.J. Miller, N.E. Miller.
Plasma-high-density-lipoprotein concentration and development of ischaemic heart-disease.
Lancet, 1 (1975), pp. 16-19
[5.]
G.J. Miller.
High density lipoproteins and atherosclerosis.
[6.]
P.N. Hopkins, R.R. Williams.
A survey of 246 suggested coronary risk factors.
Atherosclerosis, 40 (1981), pp. 1-52
[7.]
G. Assmann, H. Schulte.
Relations of high-density lipoprotein cholesterol and triglycerides to incidence of atherosclerotic coronary artery diseae (the PROCAM experience).
Am J Cardiol, 70 (1992), pp. 733-737
[8.]
S.A. Brown, R. Hutchinson, J. Morrisett, E. Boerwinkle, C.E. Davis, J.r. Gotto AM, et al.
Plasma lipid, lipoprotein cholesterol, and apoprotein distributions in selected US communities.
Arteriosclerosis Thromb, 13 (1993), pp. 1139-1142
[9.]
R. Ross.
The pathogenesis of atherosclerosis: a perspective for the 1990s.
Nature, 362 (1993), pp. 801-809
[10.]
M. Navab, J.A. Berliner, A.D. Watson, S.Y. Hama, M.C. Territo, A.J. Lusis, et al.
The Yin and Yang of oxidation in the development of the fatty streak: a review based on the 1994 George Lyman Duff Memorial Lecture.
Arterocler Thormb Vasc Biol, 16 (1996), pp. 831-842
[11.]
K.K. Griendling, R.W. Alexander.
Oxidative stress and cardiovascular disease.
Circulation, 96 (1997), pp. 3264-3265
[12.]
R. Ross.
Atherosclerosis an inflammatory disease.
N Engl J Med, 340 (1999), pp. 115-126
[13.]
C.P. Sparrow, S. Parthasarathy, D. Steinberg.
Macrophage receptor that recognizes low density lipoprotein but not acetylated low density lipoprotein.
J Biol Chem, 264 (1989), pp. 2599-2604
[14.]
A. Amberger, C. Maczek, G. Jurgens, D. Michaelis, G. Schett, K. Trieb, et al.
Co-expression of ICAM-1, VCAM-1, ELAM-1 and Hsp60 in human arterial and venous endothelial cells in response to cytokines and oxidized low-density lipoproteins.
Cell Stress Chaperones, 2 (1997), pp. 94-103
[15.]
W. Erl, P.C. Weber, C. Weber.
Monocytic cell adhesion to endothelial cells stimulated by ozidized low density lipoprotein is mediated by distinct endothelial ligands.
Atherosclerosis, 136 (1998), pp. 297-303
[16.]
M. Braun, P. Pietsch, K. Schror, G. Baumann, S.B. Felix.
Cellular adhesion molecules on vascular smooth muscle cells.
Cardiovasc Res, 41 (1999), pp. 395-401
[17.]
J.H. Lin, Y. Zhu, H.L. Liao, Y. Kobary, L. Groszek, M.B. Stemerman.
Induction of vascular cell adhesion molecule-1 by low-density lipoprotein.
Atherosclerosis, 127 (1996), pp. 185-194
[18.]
J.W. Heinecke.
Free radical modification of low density lipoproteins: mechanism and biological consequences.
Free Radic Biol Med, 3 (1987), pp. 65-73
[19.]
S. Parthasarathy, N. Auge, N. Sananam.
Impliations of lag time concept in the oxidation of LDL.
Free Radic Res, 28 (1998), pp. 583-591
[20.]
A. Wakatsuki, N. Ikenoue, Y. Sagara.
Effects of estrogen on susceptibility to oxidation of low-density and high-density lipoprotein in postmenopausal women.
Maturitas, 28 (1998), pp. 229-234
[21.]
H. Ohkawa, N. Ohishi, K. Yagi.
Assay for lipid peroxides in animal tissues by hiobarbituric acid reaction.
Anal Biochem, 95 (1979), pp. 351-358
[22.]
M.N. Bui, M.N. Sack, M.N. Moutsatsos, D.Y. Lu, P. Katz, R. McCown, et al.
Autoantibody titers to oxidized low-density lipoprotein in patients with coronary atherosclerosis.
Am Heart J, 131 (1996), pp. 663-667
[23.]
M.M.S. Shen, R.M. Krauss, F.T. Lindgern, T.M. Forte.
Heterogeneity of serum low density lipoproteins in normal human subjects.
J Lipid Res, 22 (1981), pp. 236-244
[24.]
R.M. Krauss, D.J. Burke.
Identification of multiple subclasses of plasma low density lipoproteins in normal humans.
J Lipid Res, 23 (1982), pp. 97-104
[25.]
J. De Graaf, H.L.M. Hak-Lemmers, M.P.C. Hectors, P.N.M. Demacker, J.V.M. Hendriks, A.F.H. Stalenhoef.
Enhanced susceptibility to in vitro oxidation of the dense low density lipoprotein subfraction in healthy subjects.
Arteriosclerosis, 11 (1991), pp. 298-306
[26.]
G. Camejo.
Effect of proteoglycans on lipoprotein-cell interactions: possible contributions to atherogenesis.
Curr Opin Lipidol, 1 (1990), pp. 431-436
[27.]
H. Campos, K.S. Arnold, M.E. Balestra, T.L. Innerarity, R.M. Krauss.
Differences in receptor binding of low density lipoprotein subfractions.
Arterioscler Thromb Vasc Biol, 16 (1996), pp. 794-801
[28.]
H. Campos, J.r. Genest JJ, E. Blijlevens, J.R. McNamara, J.L. Jenner, J.M. Ordovas, et al.
Low density lipoprotein particle size and coronary artery disease.
Arterioscler Thromb, 12 (1992), pp. 187-195
[29.]
J. Coresh, P.O. Kwiterovich, H.H. Smith, P.S. Bachorik.
Association of plasma triglyceride concentration and LDL particle diameter, density, and chemical composition particle with premature coronary artery disease in men and women.
J Lipid Res, 34 (1993), pp. 1687-1697
[30.]
C.D. Gardner, S.P. Fortmann, R.M. Krauss.
Association of small low-density lipoprotein particles with the incidence of coronary artery disease in men and women.
Jama, 276 (1996), pp. 875-881
[31.]
M.J. Stampfer, R.M. Krauss, J. Ma, P.J. Blanche, L.G. Holl, F.M. Sacks, et al.
A prospective study of triglyceride level, low-density lipoprotein particle diameter, and risk of myocardial infarction.
Jama, 276 (1996), pp. 882-888
[32.]
J.R. Crouse, J.S. Parks, H.M. Schey, F.R. Kahl.
Studies of low density lipoprotein molecular weight in human beings with coronary artery disease.
J Lipid Res, 26 (1985), pp. 566-574
[33.]
H. Campos, J.R. McNamara, P.W.F. Wilson, J.M. Ordovas, E.J. Schaefer.
Differences in low density lipoprotein subfractions and apolipoproteins in premenopausal and postmenopausal women.
J Clin Endocrinol Metab, 67 (1988), pp. 30-35
[34.]
N. Ikenoue, A. Wakatsuki, Y. Okatani.
Small low density lipoprotein particles in women with natural or surgically induced menopause.
Obstel Gynecol, 93 (1999), pp. 566-570
[35.]
M.A. Austin, J.E. Hokanson, K.L. Edwards.
Hypertriglyceridemia as a cardiovascular risk factor.
Am J Cardiol, 81 (1998), pp. B7-B12
[36.]
S. Acton, A. Rigotti, K.T. Landsdulz, S. Xu, H.H. Hobbs, M. Krienger.
Identification of scavenger receptor SR-BI as a high density lipoprotein receptor.
Science, 271 (1996), pp. 518-520
[37.]
T. Arai, N. Wang, M. Bezouevski, C. Welch, A.R. Tall.
Decreased atherosclerosis in heterozygous low density lipoprotein receptor- deficient mice expressing the scavenger receptor BI transgene.
J Biol Chem, 274 (1999), pp. 2366-2371
[38.]
M. Krieger.
Charting the fate of the “good cholesterol”: identification and characterization of the high-density lipoprotein receptor SR-BI.
Annu Rev Biochem, 68 (1999), pp. 523-558
[39.]
S. Acton, D. Osgood, M. Donoghue, D. Corella, M. Pocovi, A. Cenarro, et al.
Association of polymorphisms at the SR-BI gene locus with plasma lipid levels and body mass index in a white population.
Arterioscler Thromb Vasc Biol, 19 (1999), pp. 1734-1743
[40.]
Y. Nagano, H. Arai, T. Kita.
High density lipoprotein loses its effect to stimulate efflux of cholesterol from foam cells after oxidative modification.
Proc Natl Acad Sci USA, 88 (1991), pp. 6457-6461
[41.]
M.J. Albrink, E.B. Man.
Serum triglycerides in coronary artery disease.
Arch Intern Med, 103 (1959), pp. 4-8
[42.]
H. Cintora, R. Altman, A. Scazziota, F. Cintora, M. Melcon, M. Manchain, et al.
Trigliceridemia basal y riesgo cardiovascular: 150–200 mg/dl como “rango crítico” con mayor riesgo aterogénico en individuos aparentemente sanos.
Clin Invest Ateriosclerosis, 11 (1999), pp. 113-120
[43.]
The Lipid Research Clinics Coronary Primary Prevention Trial results.
I. Reduction in incidence of coronary heart disease.
Jama, 251 (1984), pp. 351-364
[44.]
J.C. Rutledge, M.M. Woo, A.A. Rezai, L.K. Curtiss, I.J. Goldberg.
Lipoprotein lipase increases lipoprotein binding to the artery wall and increases endothelial layer permeability by formation of lipolysis products.
Circ Res, 80 (1997), pp. 819-828
[45.]
M. Rath, A. Niendorf, T. Reblin, M. Dietel, H.J. Krebber, U. Beisiegel.
Detection and quantitation of lipoprotein(a) in the arterial wall of 107 coronary bypass patients.
Arteriosclerosis, 9 (1989), pp. 579-592
[46.]
E.B. Smith, S. Cochran.
Factors influencing the acumulation in fibrous plaques of lipid derived from low density lipoprotein. Preferential immobilization of lipoprotein(a).
Atherosclerosis, 84 (1990), pp. 173-181
[47.]
L.H. Hervio, V. Durlach, A. Girard-Globa, E. Anglés-Cano.
Multiple binding with identical linkage: A mechanism that explains the effect of lipoprotein(a) on fibrinolysis.
Biochemistry, 34 (1995), pp. 13353-13358
[48.]
C.J. Kim, W.S. Ryu, J.W. Kwak, C.T. Park, U.H. Ryoo.
Changes in Lp(a) lipoprotein and lipid levels after cessation of femals sex hormone production and estrogen replacement therapy.
Arch Intern Med, 156 (1996), pp. 500-504
Copyright © 2001. Sociedad Española de Ginecología y Obstetricia
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