<?xml version="1.0" encoding="UTF-8"?>
<!DOCTYPE article PUBLIC "-//NLM//DTD JATS (Z39.96) Journal Publishing DTD v1.3 20210610//EN" "JATS-journalpublishing1-3.dtd">
<article article-type="research-article" dtd-version="1.3" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xml:lang="ru"><front><journal-meta><journal-id journal-id-type="publisher-id">cardiovascular</journal-id><journal-title-group><journal-title xml:lang="ru">Кардиоваскулярная терапия и профилактика</journal-title><trans-title-group xml:lang="en"><trans-title>Cardiovascular Therapy and Prevention</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1728-8800</issn><issn pub-type="epub">2619-0125</issn><publisher><publisher-name>«SILICEA-POLIGRAF» LLC</publisher-name></publisher></journal-meta><article-meta><article-id custom-type="elpub" pub-id-type="custom">cardiovascular-1327</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>ОБЗОРЫ ЛИТЕРАТУРЫ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>REVIEW ARTICLES</subject></subj-group></article-categories><title-group><article-title>К вопросу патогенеза болезней системы кровообращения</article-title><trans-title-group xml:lang="en"><trans-title>Circulatory disease pathogenesis</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Воробьева</surname><given-names>Е. Н.</given-names></name><name name-style="western" xml:lang="en"><surname>Vorobyeva</surname><given-names>E. N.</given-names></name></name-alternatives><email xlink:type="simple">elenavorobyova@yandex.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Осипова</surname><given-names>И. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Osipova</surname><given-names>I. V.</given-names></name></name-alternatives><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Воробьев</surname><given-names>Р. И.</given-names></name><name name-style="western" xml:lang="en"><surname>Vorobyev</surname><given-names>R. I.</given-names></name></name-alternatives><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Трешутина</surname><given-names>Ю. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Treshutina</surname><given-names>Yu. V.</given-names></name></name-alternatives><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Алтайский государственный медицинский университет. Барнаул</institution></aff><aff xml:lang="en"><institution>Altay State Medical University. Barnaul,</institution></aff></aff-alternatives><pub-date pub-type="collection"><year>2006</year></pub-date><pub-date pub-type="epub"><day>20</day><month>10</month><year>2006</year></pub-date><volume>5</volume><issue>5</issue><fpage>114</fpage><lpage>120</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Воробьева Е.Н., Осипова И.В., Воробьев Р.И., Трешутина Ю.В., 2006</copyright-statement><copyright-year>2006</copyright-year><copyright-holder xml:lang="ru">Воробьева Е.Н., Осипова И.В., Воробьев Р.И., Трешутина Ю.В.</copyright-holder><copyright-holder xml:lang="en">Vorobyeva E.N., Osipova I.V., Vorobyev R.I., Treshutina Y.V.</copyright-holder><license xml:lang="ru" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>Данная работа распространяется под лицензией Creative Commons Attribution 4.0.</license-p></license><license xml:lang="en" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>This work is licensed under a Creative Commons Attribution 4.0 License.</license-p></license></permissions><self-uri xlink:href="https://cardiovascular.elpub.ru/jour/article/view/1327">https://cardiovascular.elpub.ru/jour/article/view/1327</self-uri><abstract><p>Обзор посвящен биологической роли активных форм кислорода (АФК), которые конститутивно генерируются в различных клетках здоровых организмов, от одноклеточных до высокоорганизованных, выполняя, благодаря высокой химической реактивности и весьма короткой продолжительности жизни, важную функцию сигнальных внутриклеточных трансдукторов и межклеточных медиаторов для реализации срочной и отсроченной адаптивной перестройки тканевого метаболизма, в т.ч. в системе кровообращения. При значительном накоплении в организме таких молекул их медиаторная функция трансформируется в повреждающую, обусловленную окислением и разрушением тканевых липидов, белков и нуклеиновых кислот с развитием патологических повреждений. Эта концепция согласуется с многочисленными клиническими сообщениями о том, что у больных эссенциальной гипертонией, атеросклерозом, ишемической болезнью сердца и инфарктом миокарда тканевой и плазменный уровень АФК и продуктов окислительного повреждения клеточных биополимеров во много раз выше величин, наблюдаемых у здоровых людей даже в период экстремальных ситуаций; патогенетически значимыми в данном случае выступает локальная и/или системная гиперпродукция супероксидных и гидроксильных радикалов, гидропероксида, оксида азота, пероксинитрита и других АФК.</p></abstract><trans-abstract xml:lang="en"><p>The review is devoted to biological role of reactive oxygen forms, generated in various cells of all healthy organisms, and performing, due to their high chemical reactivity and short lifetime, vital function of signal intracellular transduction and intercellular mediation, realizing immediate and delayed adaptation of tissue metabolism, circulatory system included. In excessive amount of these molecules, their moderating function transforms into damaging oxidation and destruction of tissue lipids, proteins and nucleic acids. This concept is supported by numerous clinical data on substantial increase in tissue and plasma levels of active oxygen forms and oxidative cellular biopolymer damage products among patients with essential arterial hypertension, atheroscleroisis, coronary heart disease and myocardial infarction. The leading pathogenetic role is played by local and/or systemic hyperproduction of superoxide and hydroxide radicals, hydroperoxide, NO, peroxinitrite and other active oxygen forms.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>болезни системы кровообращения</kwd><kwd>факторы риска</kwd><kwd>свободнорадикальное окисление</kwd><kwd>дислипопротеинемии</kwd></kwd-group><kwd-group xml:lang="en"><kwd>Circulatory disease</kwd><kwd>risk factors</kwd><kwd>free-radical oxidation</kwd><kwd>dyslipoproteinemia</kwd></kwd-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Чазов Е.И. Проблемы лечения больных ишемической болезнью сердца. Тер архив 2000; 9: 5-9.</mixed-citation><mixed-citation xml:lang="en">Чазов Е.И. Проблемы лечения больных ишемической болезнью сердца. Тер архив 2000; 9: 5-9.</mixed-citation></citation-alternatives></ref><ref id="cit2"><label>2</label><citation-alternatives><mixed-citation xml:lang="ru">Щепин О.П., Овчаров В.К., Какорина Е.П. Основные тенденции формирования здоровья населения Российской Федерации в 1998 г. Пробл соц гиг здравоохр ист мед 1999; 6: 3-11.</mixed-citation><mixed-citation xml:lang="en">Щепин О.П., Овчаров В.К., Какорина Е.П. Основные тенденции формирования здоровья населения Российской Федерации в 1998 г. Пробл соц гиг здравоохр ист мед 1999; 6: 3-11.</mixed-citation></citation-alternatives></ref><ref id="cit3"><label>3</label><citation-alternatives><mixed-citation xml:lang="ru">Beckman JS, Carson M, Smith CD, Koppenol WH. SLS, SOD and peroxynitrite. Nature 1993; 364: 584-7.</mixed-citation><mixed-citation xml:lang="en">Beckman JS, Carson M, Smith CD, Koppenol WH. SLS, SOD and peroxynitrite. Nature 1993; 364: 584-7.</mixed-citation></citation-alternatives></ref><ref id="cit4"><label>4</label><citation-alternatives><mixed-citation xml:lang="ru">Blumenthal JA, O,Connor C, Hinderliter A, et al. Psycho-social factors and coronary disease. A national multicenter clinical trial (ENRICHD) with a North Carolina focus. N C Med J 1997; 58: 440-4.</mixed-citation><mixed-citation xml:lang="en">Blumenthal JA, O,Connor C, Hinderliter A, et al. Psycho-social factors and coronary disease. A national multicenter clinical trial (ENRICHD) with a North Carolina focus. N C Med J 1997; 58: 440-4.</mixed-citation></citation-alternatives></ref><ref id="cit5"><label>5</label><citation-alternatives><mixed-citation xml:lang="ru">Bredt DS. Endogenous nitric oxide synthesis: biological functions and pathophysiology. Free Rad Res 1999; 31: 577-81.</mixed-citation><mixed-citation xml:lang="en">Bredt DS. Endogenous nitric oxide synthesis: biological functions and pathophysiology. Free Rad Res 1999; 31: 577-81.</mixed-citation></citation-alternatives></ref><ref id="cit6"><label>6</label><citation-alternatives><mixed-citation xml:lang="ru">Capaldo B, Guardasole V, Pardo F, et al. Abnormal Vascular Reactivity in Growth Hormone Deficiency. Circulation 2001; 103: 520-4.</mixed-citation><mixed-citation xml:lang="en">Capaldo B, Guardasole V, Pardo F, et al. Abnormal Vascular Reactivity in Growth Hormone Deficiency. Circulation 2001; 103: 520-4.</mixed-citation></citation-alternatives></ref><ref id="cit7"><label>7</label><citation-alternatives><mixed-citation xml:lang="ru">Cooke JP, Dzau VJ. Nitric oxide synthase: Role in the Genesis of Vascular Disease. Ann Rev Med 1997; 48: 489-509.</mixed-citation><mixed-citation xml:lang="en">Cooke JP, Dzau VJ. Nitric oxide synthase: Role in the Genesis of Vascular Disease. Ann Rev Med 1997; 48: 489-509.</mixed-citation></citation-alternatives></ref><ref id="cit8"><label>8</label><citation-alternatives><mixed-citation xml:lang="ru">Daugherty MO, Rich GF, Johns RA. Vascular endothelium. Cur Opin Anaesthesiol 1995; 8: 88-94.</mixed-citation><mixed-citation xml:lang="en">Daugherty MO, Rich GF, Johns RA. Vascular endothelium. Cur Opin Anaesthesiol 1995; 8: 88-94.</mixed-citation></citation-alternatives></ref><ref id="cit9"><label>9</label><citation-alternatives><mixed-citation xml:lang="ru">Finkel T. Oxygen radicals and signaling. Cur Opin Cell Biol 1998; 10: 248-53.</mixed-citation><mixed-citation xml:lang="en">Finkel T. Oxygen radicals and signaling. Cur Opin Cell Biol 1998; 10: 248-53.</mixed-citation></citation-alternatives></ref><ref id="cit10"><label>10</label><citation-alternatives><mixed-citation xml:lang="ru">Gianturco SH, Bradley WA. Atherosclerosis: cell biology and lipoproteins. Cur Opin Lipidol 1994; 5: 313-5.</mixed-citation><mixed-citation xml:lang="en">Gianturco SH, Bradley WA. Atherosclerosis: cell biology and lipoproteins. Cur Opin Lipidol 1994; 5: 313-5.</mixed-citation></citation-alternatives></ref><ref id="cit11"><label>11</label><citation-alternatives><mixed-citation xml:lang="ru">Givertz MM, Colucci WS. New targets for heart-failure therapy: endothelin, in-flammatory cytokines, and oxidative stress. Lancet 1998; 352(1): 34-8.</mixed-citation><mixed-citation xml:lang="en">Givertz MM, Colucci WS. New targets for heart-failure therapy: endothelin, in-flammatory cytokines, and oxidative stress. Lancet 1998; 352(1): 34-8.</mixed-citation></citation-alternatives></ref><ref id="cit12"><label>12</label><citation-alternatives><mixed-citation xml:lang="ru">Griendling KK, Minieri CA, Ollerenshaw JD, Alexander RW. Angiotensin II stimulates NADH and NADPH oxidase activity in cultured smooth muscle cells. Circulation Res 1994; 74: 1141-8.</mixed-citation><mixed-citation xml:lang="en">Griendling KK, Minieri CA, Ollerenshaw JD, Alexander RW. Angiotensin II stimulates NADH and NADPH oxidase activity in cultured smooth muscle cells. Circulation Res 1994; 74: 1141-8.</mixed-citation></citation-alternatives></ref><ref id="cit13"><label>13</label><citation-alternatives><mixed-citation xml:lang="ru">Halliwell B. Oxidative stress, nutrition and health. Experimental strategies for optimization of nutritional antioxidant intake in humans. Free Radic Res 1996; 25: 57-74.</mixed-citation><mixed-citation xml:lang="en">Halliwell B. Oxidative stress, nutrition and health. Experimental strategies for optimization of nutritional antioxidant intake in humans. Free Radic Res 1996; 25: 57-74.</mixed-citation></citation-alternatives></ref><ref id="cit14"><label>14</label><citation-alternatives><mixed-citation xml:lang="ru">Harrison DG. Endothelial function and oxidant stress. Clin Cardiol 1997; 20(Suppl. II): 11-7.</mixed-citation><mixed-citation xml:lang="en">Harrison DG. Endothelial function and oxidant stress. Clin Cardiol 1997; 20(Suppl. II): 11-7.</mixed-citation></citation-alternatives></ref><ref id="cit15"><label>15</label><citation-alternatives><mixed-citation xml:lang="ru">Howarth P. H Pathogenic mechanisms: a rational basis for treatment. BMJ 1998; 316: 758-61.</mixed-citation><mixed-citation xml:lang="en">Howarth P. H Pathogenic mechanisms: a rational basis for treatment. BMJ 1998; 316: 758-61.</mixed-citation></citation-alternatives></ref><ref id="cit16"><label>16</label><citation-alternatives><mixed-citation xml:lang="ru">Hwang SJ, Ballantyne CM, Sharrett AR, et al. Circulating adhesion molecules VCAM-1, ICAM-1, and E-selectin in carotid atherosclerosis and incident coronary heart disease cases (ARIC). Circulation 1997; 96: 4219-25.</mixed-citation><mixed-citation xml:lang="en">Hwang SJ, Ballantyne CM, Sharrett AR, et al. Circulating adhesion molecules VCAM-1, ICAM-1, and E-selectin in carotid atherosclerosis and incident coronary heart disease cases (ARIC). Circulation 1997; 96: 4219-25.</mixed-citation></citation-alternatives></ref><ref id="cit17"><label>17</label><citation-alternatives><mixed-citation xml:lang="ru">Kasim-Karakas SE. Impact of n-3 fatty acids on lipoprotein metabolism. Cur Opin Lipidol 1995; 6: 167-71.</mixed-citation><mixed-citation xml:lang="en">Kasim-Karakas SE. Impact of n-3 fatty acids on lipoprotein metabolism. Cur Opin Lipidol 1995; 6: 167-71.</mixed-citation></citation-alternatives></ref><ref id="cit18"><label>18</label><citation-alternatives><mixed-citation xml:lang="ru">Laursen JB, Rajagopalan S, Galis Z, et al. Role of superoxide in angiotensin II-induced but not catecholamine-induced hypertension. Circulation 1997; 95: 588-93.</mixed-citation><mixed-citation xml:lang="en">Laursen JB, Rajagopalan S, Galis Z, et al. Role of superoxide in angiotensin II-induced but not catecholamine-induced hypertension. Circulation 1997; 95: 588-93.</mixed-citation></citation-alternatives></ref><ref id="cit19"><label>19</label><citation-alternatives><mixed-citation xml:lang="ru">Lavreni A, Salobir BG, Keber I, et al. Physical Training Improves Flow-Mediated Dilation in Patients With the Polymetabolic Syndrome. Arterioscl Thromb Vasc Biol 2000; 20: 551-9.</mixed-citation><mixed-citation xml:lang="en">Lavreni A, Salobir BG, Keber I, et al. Physical Training Improves Flow-Mediated Dilation in Patients With the Polymetabolic Syndrome. Arterioscl Thromb Vasc Biol 2000; 20: 551-9.</mixed-citation></citation-alternatives></ref><ref id="cit20"><label>20</label><citation-alternatives><mixed-citation xml:lang="ru">Li H, Forstermann U. Nitric oxide in the pathogenesis of vascular disease. J Pathol 2000; 190: 244-54, 319-26.</mixed-citation><mixed-citation xml:lang="en">Li H, Forstermann U. Nitric oxide in the pathogenesis of vascular disease. J Pathol 2000; 190: 244-54, 319-26.</mixed-citation></citation-alternatives></ref><ref id="cit21"><label>21</label><citation-alternatives><mixed-citation xml:lang="ru">Luscher TF, Noll G, Vanhoutte PM. Endothelial dysfunction in hypertension. J Hypertens 1996: 14(5): 383-93.</mixed-citation><mixed-citation xml:lang="en">Luscher TF, Noll G, Vanhoutte PM. Endothelial dysfunction in hypertension. J Hypertens 1996: 14(5): 383-93.</mixed-citation></citation-alternatives></ref><ref id="cit22"><label>22</label><citation-alternatives><mixed-citation xml:lang="ru">Nathan CF. Secretory products of macrophages. J Clin Invest 1987; 79: 319-26.</mixed-citation><mixed-citation xml:lang="en">Nathan CF. Secretory products of macrophages. J Clin Invest 1987; 79: 319-26.</mixed-citation></citation-alternatives></ref><ref id="cit23"><label>23</label><citation-alternatives><mixed-citation xml:lang="ru">Nathan CF, Ortenblad N, Madsen K, Djurhuus MS. Antioxidant status and lipid peroxi-dation after short-term maximal exercise in trained and untrained humans. Am J Physiol 1997; 272(4): 1258-63.</mixed-citation><mixed-citation xml:lang="en">Nathan CF, Ortenblad N, Madsen K, Djurhuus MS. Antioxidant status and lipid peroxi-dation after short-term maximal exercise in trained and untrained humans. Am J Physiol 1997; 272(4): 1258-63.</mixed-citation></citation-alternatives></ref><ref id="cit24"><label>24</label><citation-alternatives><mixed-citation xml:lang="ru">Ouchi N, Kihara S, Arita Y, et al. Adipocyte-Derived Plasma Protein, Adiponectin, Suppresses Lipid Accumulation and Class A Scavenger Receptor Expression in Human Monocyte-Derived Macrophages. Circulation 2001; 103: 1057-63.</mixed-citation><mixed-citation xml:lang="en">Ouchi N, Kihara S, Arita Y, et al. Adipocyte-Derived Plasma Protein, Adiponectin, Suppresses Lipid Accumulation and Class A Scavenger Receptor Expression in Human Monocyte-Derived Macrophages. Circulation 2001; 103: 1057-63.</mixed-citation></citation-alternatives></ref><ref id="cit25"><label>25</label><citation-alternatives><mixed-citation xml:lang="ru">Parthasarathy S, Santanam N. Potential Role of Oxidized Lipids and Lipoproteins in Antioxidant Defense. Free Rad Res 2000; 33: 197-215.</mixed-citation><mixed-citation xml:lang="en">Parthasarathy S, Santanam N. Potential Role of Oxidized Lipids and Lipoproteins in Antioxidant Defense. Free Rad Res 2000; 33: 197-215.</mixed-citation></citation-alternatives></ref><ref id="cit26"><label>26</label><citation-alternatives><mixed-citation xml:lang="ru">Ross R. The Pathogenesis of Atherosclerosis: An Update. Atherosclerosis Beyond Cholesterd. Hanover 1992; 17 p.</mixed-citation><mixed-citation xml:lang="en">Ross R. The Pathogenesis of Atherosclerosis: An Update. Atherosclerosis Beyond Cholesterd. Hanover 1992; 17 p.</mixed-citation></citation-alternatives></ref><ref id="cit27"><label>27</label><citation-alternatives><mixed-citation xml:lang="ru">Sanchez-Quesada JLR, Homs-Serradesanferm J, Serrat-Serrat JR, et al. Increase of LDL susceptibility to oxidation occurring after intense, long duration aerobic exercise. Atherosclerosis 1995; 118: 297-305.</mixed-citation><mixed-citation xml:lang="en">Sanchez-Quesada JLR, Homs-Serradesanferm J, Serrat-Serrat JR, et al. Increase of LDL susceptibility to oxidation occurring after intense, long duration aerobic exercise. Atherosclerosis 1995; 118: 297-305.</mixed-citation></citation-alternatives></ref><ref id="cit28"><label>28</label><citation-alternatives><mixed-citation xml:lang="ru">Scandinavian Simvastatin Survival Study Group. Randomized trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet 1994; 344: 1383-9.</mixed-citation><mixed-citation xml:lang="en">Scandinavian Simvastatin Survival Study Group. Randomized trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet 1994; 344: 1383-9.</mixed-citation></citation-alternatives></ref><ref id="cit29"><label>29</label><citation-alternatives><mixed-citation xml:lang="ru">Sen-Banerjee S, Siles X, Campos H. Tobacco Smoking Modifies Association Between Gln-Arg192 Polymorphism of Human Paraoxonase Gene and Risk of Myocardial Infarction. Arterioscl Thromb Vasc Biol 2000; 20: 2120-8.</mixed-citation><mixed-citation xml:lang="en">Sen-Banerjee S, Siles X, Campos H. Tobacco Smoking Modifies Association Between Gln-Arg192 Polymorphism of Human Paraoxonase Gene and Risk of Myocardial Infarction. Arterioscl Thromb Vasc Biol 2000; 20: 2120-8.</mixed-citation></citation-alternatives></ref><ref id="cit30"><label>30</label><citation-alternatives><mixed-citation xml:lang="ru">Shephard G, Cobbe SM, Ford J, еt al. Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. West of Scotland Coronary Prevention Study Group (WOSCOPS). N Engl J Med 1995; 333: 1301-7.</mixed-citation><mixed-citation xml:lang="en">Shephard G, Cobbe SM, Ford J, еt al. Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. West of Scotland Coronary Prevention Study Group (WOSCOPS). N Engl J Med 1995; 333: 1301-7.</mixed-citation></citation-alternatives></ref><ref id="cit31"><label>31</label><citation-alternatives><mixed-citation xml:lang="ru">Spiecker M, Peng HB, Liao JK. Inhibition of endothelial vascular cell adhesion molecule-1 expression by nitric oxide involves the induction and nuclear translocation of NfkB. J Biol Chem 1997; 272: 30969-74.</mixed-citation><mixed-citation xml:lang="en">Spiecker M, Peng HB, Liao JK. Inhibition of endothelial vascular cell adhesion molecule-1 expression by nitric oxide involves the induction and nuclear translocation of NfkB. J Biol Chem 1997; 272: 30969-74.</mixed-citation></citation-alternatives></ref><ref id="cit32"><label>32</label><citation-alternatives><mixed-citation xml:lang="ru">Stamler J. Established major coronary risk factors. In Coronary heart disease epidemiology. Eds. Marmot M., Elliott P. Oxford University Press 1996; 35-62.</mixed-citation><mixed-citation xml:lang="en">Stamler J. Established major coronary risk factors. In Coronary heart disease epidemiology. Eds. Marmot M., Elliott P. Oxford University Press 1996; 35-62.</mixed-citation></citation-alternatives></ref><ref id="cit33"><label>33</label><citation-alternatives><mixed-citation xml:lang="ru">Stangl H, Hyatt M, Hobbs H. Transport of Lipids from High and Low Density Lipoproteins via Scavenger Receptor-BI. J Biol Chem 1999; 274(Issue 46): 32692-8.</mixed-citation><mixed-citation xml:lang="en">Stangl H, Hyatt M, Hobbs H. Transport of Lipids from High and Low Density Lipoproteins via Scavenger Receptor-BI. J Biol Chem 1999; 274(Issue 46): 32692-8.</mixed-citation></citation-alternatives></ref><ref id="cit34"><label>34</label><citation-alternatives><mixed-citation xml:lang="ru">Steinberg D. Low Density Lipoprotein Oxidation and Its Pathobiological Significance. J Biol Chem 1997: 272(34): 20963-6.</mixed-citation><mixed-citation xml:lang="en">Steinberg D. Low Density Lipoprotein Oxidation and Its Pathobiological Significance. J Biol Chem 1997: 272(34): 20963-6.</mixed-citation></citation-alternatives></ref><ref id="cit35"><label>35</label><citation-alternatives><mixed-citation xml:lang="ru">Vincent HK, Powers SK, Stewart DJ, et al. Obesity is associated with increased myocardial oxidative stress. Dept. of Exercise Sport Sci., Center Exercise Sci., Univ. of Florida, Gainesville, USA. Int J Obes Relat Metab Disord 1999; 23: 67-74.</mixed-citation><mixed-citation xml:lang="en">Vincent HK, Powers SK, Stewart DJ, et al. Obesity is associated with increased myocardial oxidative stress. Dept. of Exercise Sport Sci., Center Exercise Sci., Univ. of Florida, Gainesville, USA. Int J Obes Relat Metab Disord 1999; 23: 67-74.</mixed-citation></citation-alternatives></ref><ref id="cit36"><label>36</label><citation-alternatives><mixed-citation xml:lang="ru">Yokode M, Ueyama K, Arai NH, et al. Modification of high- and low-density lipoproteins by cigarette smoke oxidants. Ann N-Y Acad Sci 1996; 786: 245-51.</mixed-citation><mixed-citation xml:lang="en">Yokode M, Ueyama K, Arai NH, et al. Modification of high- and low-density lipoproteins by cigarette smoke oxidants. Ann N-Y Acad Sci 1996; 786: 245-51.</mixed-citation></citation-alternatives></ref><ref id="cit37"><label>37</label><citation-alternatives><mixed-citation xml:lang="ru">Zafari AM, Ushio-Fukai M, Akers M et al. Role of NADH/ NADPH oxidase-derived H2O2 in angiotensin II-induced vascular hypertrophy. Hypertension 1998; 32(30): 488-95.</mixed-citation><mixed-citation xml:lang="en">Zafari AM, Ushio-Fukai M, Akers M et al. Role of NADH/ NADPH oxidase-derived H2O2 in angiotensin II-induced vascular hypertrophy. Hypertension 1998; 32(30): 488-95.</mixed-citation></citation-alternatives></ref></ref-list><fn-group><fn fn-type="conflict"><p>The authors declare that there are no conflicts of interest present.</p></fn></fn-group></back></article>
