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<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">rsp</journal-id><journal-title-group><journal-title xml:lang="ru">Научно-практическая ревматология</journal-title><trans-title-group xml:lang="en"><trans-title>Rheumatology Science and Practice</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1995-4484</issn><issn pub-type="epub">1995-4492</issn><publisher><publisher-name>IMA-PRESS, LLC</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.14412/1995-4484-2018-28-34</article-id><article-id custom-type="elpub" pub-id-type="custom">rsp-2687</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>ОРИГИНАЛЬНЫЕ ИССЛЕДОВАНИЯ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>ORIGINAL RESEARCH</subject></subj-group></article-categories><title-group><article-title>Роль интерлейкина 1 в развитии атеросклероза</article-title><trans-title-group xml:lang="en"><trans-title>Role of interleukin 1 in the development of atherosclerosis</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>Насонов</surname><given-names>Е. Л.</given-names></name><name name-style="western" xml:lang="en"><surname>Nasonov</surname><given-names>E. L.</given-names></name></name-alternatives><bio xml:lang="ru"><p>115522 Москва, Каширское шоссе, 34А;</p><p>кафедра ревматологии Института профессионального образования, 119991 Москва, ул. Трубецкая, 8, стр. 2</p></bio><bio xml:lang="en"><p>34A, Kashirskoe Shosse, Moscow 115522;</p><p>8, Trubetskaya St., Build. 2, Moscow 119991</p></bio><email xlink:type="simple">nasonov@irramn.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>Попкова</surname><given-names>Т. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Popkova</surname><given-names>T. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>115522 Москва, Каширское шоссе, 34А</p></bio><bio xml:lang="en"><p>34A, Kashirskoe Shosse, Moscow 115522</p></bio><xref ref-type="aff" rid="aff-2"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>ФГБНУ «Научно-исследовательский институт ревматологии им. В.А. Насоновой»;&#13;
ФГАОУ ВО «Первый Московский государственный медицинский университет им. И.М. Сеченова» Минздрава России (Сеченовский Университет)</institution><country>Россия</country></aff><aff xml:lang="en"><institution>V.A. Nasonova Research Institute of Rheumatology;&#13;
Department of Rheumatology, Institute of Professional Education, I.M. Sechenov First Moscow State Medical University (Sechenov University), Ministry of Health of Russia</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>ФГБНУ «Научно-исследовательский институт ревматологии им. В.А. Насоновой»</institution><country>Россия</country></aff><aff xml:lang="en"><institution>V.A. Nasonova Research Institute of Rheumatology</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2018</year></pub-date><pub-date pub-type="epub"><day>03</day><month>04</month><year>2019</year></pub-date><volume>56</volume><issue>0</issue><issue-title>приложение 4</issue-title><fpage>28</fpage><lpage>34</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Насонов Е.Л., Попкова Т.В., 2019</copyright-statement><copyright-year>2019</copyright-year><copyright-holder xml:lang="ru">Насонов Е.Л., Попкова Т.В.</copyright-holder><copyright-holder xml:lang="en">Nasonov E.L., Popkova T.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://rsp.mediar-press.net/rsp/article/view/2687">https://rsp.mediar-press.net/rsp/article/view/2687</self-uri><abstract><p>В настоящее время атеросклероз рассматривается как хроническое воспалительное заболевание сосудов, связанное с «патологической» активацией врожденного и приобретенного иммунитета, характеризующееся отложением липидов, лейкоцитарной инфильтрацией и пролиферацией сосудистых гладкомышечных клеток. Субклиническое (low grade) воспаление играет фундаментальную роль на всех стадиях прогрессирования атеросклеротического процесса и определяет развитие кардиоваскулярных катастроф и летальности. Среди многочисленных медиаторов, участвующих в иммунопатогенезе как атеросклероза, так и РА, важное место занимают такие «провоспалительные» цитокины, как интерлейкин 1 (ИЛ1), ИЛ6, фактор некроза опухоли α (ФНОα), ИЛ17, ИЛ18, ИЛ27, ИЛ33, ИЛ37, тесно взаимодействующие друг с другом в рамках «цитокиновой» сети. Особое внимание привлекает ИЛ1β, играющий важную роль в развитии многих острых и хронических иммуновоспалительных заболеваний. ИЛ1β в развитии атеросклероза определяется многими механизмами, такими как «прокоагулянтная» активность, усиление адгезии моноцитов и лейкоцитов к сосудистому эндотелию, роста сосудистых гладкомышечных клеток и др. В качестве прямого доказательства фундаментальной роли воспаления в развитии атеросклероза особый интерес представляют исследования «антиатеросклеротических» эффектов препарата канакинумаб. Особый интерес представляет рандомизированное плацебоконтролируемое исследование CANTOS (Canakinumab ANti-inflammatory Thrombosis Otcomes Study), посвященное изучению эффективности терапии канакинумабом как нового подхода к вторичной профилактике кардиоваскулярных осложнений в общей популяции больных с тяжелым атеросклеротическим поражением сосудов. Результаты исследования CANTOS в сочетании со знаниями, накопленными в ревматологии в отношении кардиоваскулярных эффектов противовоспалительных препаратов, имеют огромное значение для персонификации подходов к вторичной профилактике связанных с атеросклерозом кардиоваскулярных осложнений и вносит вклад в развитие «воспалительной» теории патогенеза атеросклероза в целом.</p></abstract><trans-abstract xml:lang="en"><p>Atherosclerosis is now considered as chronic inflammatory vascular disease connected to «pathological» activation of innate and adaptive immunity, characterized by lipid deposition, leukocyte infiltration and proliferation of vascular smooth muscle cells. Subclinical (low grade) inflammation plays fundamental role at all stages of atherosclerotic process progression and determines cardiovascular catastrophes development and mortality. Proinflammatory cytokines including interleukin (IL) 1, IL6, tumor necrosis factor α (TNFα), IL17, IL18, IL27, IL33, IL37 tightly interacting within cytokine network occupy an important place among numerous mediators participating in immunopathogenesis of atherosclerosis and rheumatoid arthritis. IL1β playing an important role in the development of many acute and chronic immunoinflammatory diseases attracts particular attention. IL1β significance in the development of atherosclerosis is determined by many mechanisms including procoagulant activity, enhancement of monocytes and leucocytes adhesion to vascular endothelium, vascular smooth muscle cells growth and others. Fundamental role of inflammation in the development of atherosclerosis is well proved in investigations of anti-atherosclerotic effect of canakinumab. Randomized placebo-controlled trial CANTOS (Canakinumab ANti-inflammatory Thrombosis Otcomes Study) assessing efficacy of canakinumab as new tool for secondary prophylaxis cardiovascular complications in general population of patients with severe atherosclerotic vascular damage. CANTOS results in combination with accumulated in rheumatology data on cardiovascular effects of anti-inflammatory drugs are of great importance for personification of approach to secondary prophylaxis of caused by atherosclerosis cardiovascular complications. They also contribute to the development of inflammatory theory of atherosclerosis pathogenesis in the whole.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>атеросклероз</kwd><kwd>ревматоидный артрит</kwd><kwd>подагра</kwd><kwd>цитокины</kwd><kwd>интерлейкин 1β</kwd><kwd>канакинумаб</kwd><kwd>колхицин</kwd></kwd-group><kwd-group xml:lang="en"><kwd>atherosclerosis</kwd><kwd>rheumatoid arthritis</kwd><kwd>gout</kwd><kwd>cytokines</kwd><kwd>interleukin 1</kwd><kwd>canakinumab</kwd><kwd>colchicine</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">Ross R. Atherosclerosis – an inflammatory disease. N Engl J Med. 1999;340:S419-20. doi: 10.1016/S0002-8703(99)70266-8</mixed-citation><mixed-citation xml:lang="en">Ross R. Atherosclerosis – an inflammatory disease. 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