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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">vavilov</journal-id><journal-title-group><journal-title xml:lang="ru">Вавиловский журнал генетики и селекции</journal-title><trans-title-group xml:lang="en"><trans-title>Vavilov Journal of Genetics and Breeding</trans-title></trans-title-group></journal-title-group><issn pub-type="epub">2500-3259</issn><publisher><publisher-name>Institute of Cytology and Genetics of Siberian Branch of the RAS</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.18699/VJ21.062</article-id><article-id custom-type="elpub" pub-id-type="custom">vavilov-3113</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>МОЛЕКУЛЯРНАЯ И КЛЕТОЧНАЯ БИОЛОГИЯ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>MOLECULAR AND CELL BIOLOGY</subject></subj-group></article-categories><title-group><article-title>Механочувствительные молекулярные взаимодействия в атерогенных районах артерий: развитие атеросклероза</article-title><trans-title-group xml:lang="en"><trans-title>Mechanosensitive molecular interactions in atherogenic regions of the arteries: 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>Мищенко</surname><given-names>Е. Л.</given-names></name><name name-style="western" xml:lang="en"><surname>Mishchenko</surname><given-names>E. L.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Новосибирск</p></bio><bio xml:lang="en"><p>Novosibirsk</p></bio><email xlink:type="simple">elmish@bionet.nsc.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>Мищенко</surname><given-names>А. М.</given-names></name><name name-style="western" xml:lang="en"><surname>Mishchenko</surname><given-names>A. M.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Новосибирск</p></bio><bio xml:lang="en"><p>Novosibirsk</p></bio><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Иванисенко</surname><given-names>В. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Ivanisenko</surname><given-names>V. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Новосибирск</p></bio><bio xml:lang="en"><p>Novosibirsk</p></bio><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru">Федеральный исследовательский центр Институт цитологии и генетики Сибирского отделения Российской академии наук<country>Россия</country></aff><aff xml:lang="en">Institute of Cytology and Genetics of the Siberian Branch of the Russian Academy of Sciences<country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru">Новосибирский национальный исследовательский государственный университет<country>Россия</country></aff><aff xml:lang="en">Novosibirsk State University<country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2021</year></pub-date><pub-date pub-type="epub"><day>10</day><month>09</month><year>2021</year></pub-date><volume>25</volume><issue>5</issue><elocation-id>552­-561</elocation-id><permissions><copyright-statement>Copyright &amp;#x00A9; Мищенко Е.Л., Мищенко А.М., Иванисенко В.А., 2021</copyright-statement><copyright-year>2021</copyright-year><copyright-holder xml:lang="ru">Мищенко Е.Л., Мищенко А.М., Иванисенко В.А.</copyright-holder><copyright-holder xml:lang="en">Mishchenko E.L., Mishchenko A.M., Ivanisenko V.A.</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://vavilov.elpub.ru/jour/article/view/3113">https://vavilov.elpub.ru/jour/article/view/3113</self-uri><abstract><p>Атеросклероз, грозное заболевание сердечно­сосудистой системы, развивается в местах изгибов и разветвлений артерий, где меняются направление и модуль вектора скорости тока крови, а следовательно, механическое воздействие на контактирующие с током крови эндотелиальные клетки. Обзор посвящен актуальным исследованиям развития атеросклероза: механобиохимическим событиям, преобразующим проатерогенный механический стимул тока крови – низкое и низкое/осциллирующее напряжение сдвига, оказываемое на стенки артерий, – в цепи биохимических реакций в эндотелиальных клетках, приводящих к экспрессии специфичных белков, вызывающих прогрессирование патологического процесса. Описаны стадии, системные факторы риска, а также важный гемодинамический фактор атерогенеза: низкое и низкое/осциллирующее напряжение сдвига, оказываемое током крови на эндотелиальные клетки, выстилающие стенки артерий. Показаны взаимодействия молекул клеточной адгезии, ответственные за развитие атеросклероза в условиях низкого и низкого/осциллирующего напряжения сдвига. Описаны активация регулятора экспрессии молекул клеточной адгезии – транскрипционного фактора NF­κB – и факторы, контролирующие его активацию в этих условиях. Описаны механочувствительные сигнальные пути, приводящие к экспрессии NF­κB в эндотелиальных клетках. Исследования механобиохимических сигнальных путей и взаимодействий, вовлеченных в прогрессирование атеросклероза, необходимы для разработки подходов, задерживающих или блокирующих развитие заболевания.</p></abstract><trans-abstract xml:lang="en"><p>A terrible disease of the cardiovascular system, atherosclerosis, develops in the areas of bends and branches of arteries, where the direction and modulus of the blood flow velocity vector change, and consequently so does the mechanical effect on endothelial cells in contact with the blood flow. The review focuses on topical research studies on the development of atherosclerosis – mechanobiochemical events that transform the proatherogenic mechanical stimulus of blood flow – low and low/oscillatory arterial wall shear stress in the chains of biochemical reactions in endothelial cells, leading to the expression of specific proteins that cause the progression of the pathological process. The stages of atherogenesis, systemic risk factors for atherogenesis and its important hemodynamic factor, low and low/oscillatory wall shear stress exerted by blood flow on the endothelial cells lining the arterial walls, have been described. The interactions of cell adhesion molecules responsible for the development of atherosclerosis under low and low/oscillating shear stress conditions have been demonstrated. The activation of the regulator of the expression of cell adhesion molecules, the transcription factor NF­κB, and the factors regulating its activation under these conditions have been described. Mechanosensitive signaling pathways leading to the expression of NF­κB in endothelial cells have been described. Studies of the mechanobiochemical signaling pathways and interactions involved in the progression of atherosclerosis provide valuable information for the development of approaches that delay or block the development of this disease.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>атерогенез</kwd><kwd>напряжение сдвига</kwd><kwd>транскрипционный фактор NF­κB</kwd><kwd>экспрессия RelA</kwd><kwd>механочувствительные рецепторы</kwd><kwd>молекулы клеточной адгезии</kwd><kwd>сигнальные пути</kwd><kwd>механотрансдукция</kwd></kwd-group><kwd-group xml:lang="en"><kwd>atherogenesis</kwd><kwd>shear stress</kwd><kwd>transcription factor NF­κB</kwd><kwd>RelA expression</kwd><kwd>mechanosensitive receptors</kwd><kwd>cell adhesion molecules</kwd><kwd>signaling pathways</kwd><kwd>mechanotransduction</kwd></kwd-group><funding-group xml:lang="en"><funding-statement>The work was carried out with the support of a budget project No. 0259­2021­0009.</funding-statement></funding-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Alcaide P., Newton G., Auerbach S., Sehrawat S., Mayadas T.N., Golan D.E., Yacono P., Vincent P., Kowalczyk A., Luscinskas F.W. p120-Catenin regulates leukocyte transmigration through an effect on VE-cadherin phosphorylation. 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