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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">kpccz</journal-id><journal-title-group><journal-title xml:lang="ru">Комплексные проблемы сердечно-сосудистых заболеваний</journal-title><trans-title-group xml:lang="en"><trans-title>Complex Issues of Cardiovascular Diseases</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2306-1278</issn><issn pub-type="epub">2587-9537</issn><publisher><publisher-name>Federal State Budgetary Institution “Research Institute for Complex Issues of Cardiovascular Diseases”</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.17802/2306-1278-2017-1-92-101</article-id><article-id custom-type="elpub" pub-id-type="custom">kpccz-268</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>ОБЗОР ЛИТЕРАТУРЫ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>REVIEW ARTICLE</subject></subj-group></article-categories><title-group><article-title>РОЛЬ МУТАГЕНЕЗА В РАЗВИТИИ АТЕРОСКЛЕРОЗА</article-title><trans-title-group xml:lang="en"><trans-title>THE ROLE OF MUTAGENESIS IN 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>КУТИХИН</surname><given-names>А. Г.</given-names></name><name name-style="western" xml:lang="en"><surname>KUTIKHIN</surname><given-names>A. G.</given-names></name></name-alternatives><bio xml:lang="ru"><p>650002, г. Кемерово, Сосновый бульвар, д. 6 Тел. +79609077067</p></bio><bio xml:lang="en"><p>6, Sosnoviy blvd., Kemerovo, 650002, Russian Federation Tel. +79609077067</p></bio><email xlink:type="simple">antonkutikhin@gmail.com</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>СИНИЦКИЙ</surname><given-names>М. Ю.</given-names></name><name name-style="western" xml:lang="en"><surname>SINITSKY</surname><given-names>M. Y.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Кемерово, Россия</p></bio><bio xml:lang="en"><p>Kemerovo, Russia</p></bio><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>ПОНАСЕНКО</surname><given-names>А. В.</given-names></name><name name-style="western" xml:lang="en"><surname>PONASENKO</surname><given-names>A. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Кемерово, Россия</p></bio><bio xml:lang="en"><p>Kemerovo, Russia</p></bio><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru">Федеральное государственное бюджетное научное учреждение «Научно-исследовательский институт комплексных проблем сердечно-сосудистых заболеваний»<country>Россия</country></aff><aff xml:lang="en">Federal State Budgetary Institution Research Institute for Complex Issues of Cardiovascular Diseases<country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2017</year></pub-date><pub-date pub-type="epub"><day>08</day><month>06</month><year>2017</year></pub-date><volume>0</volume><issue>1</issue><fpage>92</fpage><lpage>101</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; КУТИХИН А.Г., СИНИЦКИЙ М.Ю., ПОНАСЕНКО А.В., 2017</copyright-statement><copyright-year>2017</copyright-year><copyright-holder xml:lang="ru">КУТИХИН А.Г., СИНИЦКИЙ М.Ю., ПОНАСЕНКО А.В.</copyright-holder><copyright-holder xml:lang="en">KUTIKHIN A.G., SINITSKY M.Y., PONASENKO A.V.</copyright-holder><license 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://www.nii-kpssz.com/jour/article/view/268">https://www.nii-kpssz.com/jour/article/view/268</self-uri><abstract><p>Атеросклероз, развивающийся в результате вызванного дисфункцией эндотелия внутрисосудистого воспаления и клинически проявляющийся ишемической болезнью сердца, острым нарушением мозгового кровообращения и заболеваниями периферических артерий, продолжает оставаться абсолютно ведущей причиной смертности. За последние четыре десятилетия было накоплено достаточно доказательств роли эндогенного и экзогенного мутагенеза в развитии атеросклероза, что позволяет рассматривать это заболевание как в некоторой степени неопластический процесс. В данном обзоре кратко освещены классические работы в этом направлении и описаны основные аргументы, подтверждающие связь мутагенеза и атеросклероза. К наиболее весомым аргументам можно отнести стимулирование развития атеросклероза активными формами кислорода, нарушение регуляции длины теломер при атеросклерозе и ускоренное развитие атеросклероза у пациентов с наследственными синдромами нарушения репарации ДНК, а также у больных, перенесших химиотерапию и лучевую терапию. Кроме того, проанализированы возможные терапевтические применения знаний о роли мутагенеза в развитии атеросклероза; в частности, подчеркнут антимутагенный эффект статинов и ингибиторов ангиотензинпревращающего фермента, что может быть дополнительной причиной их эффективности в терапии клинических осложнений атеросклероза.</p></abstract><trans-abstract xml:lang="en"><p>Atherosclerosis causing by endothelial dysfunction following vascular inflammation can lead to thrombosis and artery occlusion, resulting in myocardial infarction, ischemic stroke, or peripheral artery disease. There is a convincing evidence on the impact of endogenous and exogenous mutagenesis in atherosclerosis; therefore, it can be partially considered as a neoplastic process. Here we describe the seminal papers in the field and provide the arguments on the association of mutagenesis with atherosclerosis. In particular, we underline the importance of oxidative stress, telomere dysfunction, DNA damage syndromes, and cytotoxic chemotherapy/radiotherapy. We also consider the therapeutical applications of antimutagens, particularly statins and angiotensin-converting enzyme inhibitors.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>атеросклероз</kwd><kwd>мутагенез</kwd><kwd>мутации</kwd><kwd>репарация ДНК</kwd><kwd>статины</kwd><kwd>ингибиторы АПФ</kwd></kwd-group><kwd-group xml:lang="en"><kwd>atherosclerosis</kwd><kwd>mutagenesis</kwd><kwd>mutations</kwd><kwd>DNA repair</kwd><kwd>statins</kwd><kwd>angiotensin-converting enzyme inhibitors</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">GBD 2013 Mortality and Causes of Death Collaborators. 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