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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">10.17802/2306-1278-2024-13-3-28-36</article-id><article-id custom-type="elpub" pub-id-type="custom">kpccz-1022</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. Кардиология. Патологическая физиология</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>ORIGINAL STUDIES. Cardiology. Pathlogical physiology</subject></subj-group></article-categories><title-group><article-title>СВЯЗЬ ДЛИНЫ ТЕЛОМЕР С МАРКЕРАМИ МЕТАБОЛИЗМА И ВОСПАЛЕНИЯ В ПРЕ- И ПОСЛЕОПЕРАЦИОННОМ ПЕРИОДЕ У ПАЦИЕНТОВ С ИШЕМИЧЕСКОЙ БОЛЕЗНЬЮ СЕРДЦА</article-title><trans-title-group xml:lang="en"><trans-title>RELATIONSHIP BETWEEN TELOMERE LENGTH AND MARKERS OF INFLAMMATION IN THE PRE- AND POSTOPERATIVE PERIOD OF PATIENTS WITH CORONARY ARTERY DISEASE</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-0747-2495</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Асанов</surname><given-names>Максим Айдарович</given-names></name><name name-style="western" xml:lang="en"><surname>Asanov</surname><given-names>Maxim A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>младший научный сотрудник лаборатории геномной медицины отдела экспериментальной медицины федерального государственного бюджетного научного учреждения «Научно-исследовательский институт комплексных проблем сердечно-сосудистых заболеваний», Кемерово, Российская Федерация</p></bio><bio xml:lang="en"><p>Junior Researcher at the Laboratory of Genomic Medicine, Department of Experimental Medicine, Federal State Budgetary Institution “Research Institute for Complex Issues of Cardiovascular Diseases”, Kemerovo, Russian Federation</p></bio><email xlink:type="simple">asmaks988@gmail.com</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-7388-356X</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Поддубняк</surname><given-names>Алена Олеговна</given-names></name><name name-style="western" xml:lang="en"><surname>Poddubnyak</surname><given-names>Alyona O.</given-names></name></name-alternatives><bio xml:lang="ru"><p>младший научный сотрудник лаборатории геномной медицины отдела экспериментальной медицины федерального государственного бюджетного научного учреждения «Научно-исследовательский институт комплексных проблем сердечно-сосудистых заболеваний», Кемерово, Российская Федерация</p></bio><bio xml:lang="en"><p>Junior Researcher at the Laboratory of Genomic Medicine, Department of Experimental Medicine, Federal State Budgetary Institution “Research Institute for Complex Issues of Cardiovascular Diseases”, Kemerovo, Russian Federation</p></bio><email xlink:type="simple">alyona.poddubnyak@gmail.com</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-3002-2863</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Понасенко</surname><given-names>Анастасия Валериевна</given-names></name><name name-style="western" xml:lang="en"><surname>Ponasenko</surname><given-names>Anastasia V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>заведующая лабораторией геномной медицины отдела экспериментальной медицины федерального государственного бюджетного научного учреждения «Научно-исследовательский институт комплексных проблем сердечно-сосудистых заболеваний», Кемерово, Российская Федерация</p></bio><bio xml:lang="en"><p>Head of the Laboratory of Genomic Medicine, Department of Experimental Medicine, Federal State Budgetary Institution “Research Institute for Complex Issues of Cardiovascular Diseases”, Kemerovo, Russian Federation</p></bio><email xlink:type="simple">avapanass@mail.com</email><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>2024</year></pub-date><pub-date pub-type="epub"><day>30</day><month>09</month><year>2024</year></pub-date><volume>13</volume><issue>3</issue><fpage>28</fpage><lpage>36</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Асанов М.А., Поддубняк А.О., Понасенко А.В., 2024</copyright-statement><copyright-year>2024</copyright-year><copyright-holder xml:lang="ru">Асанов М.А., Поддубняк А.О., Понасенко А.В.</copyright-holder><copyright-holder xml:lang="en">Asanov M.A., Poddubnyak A.O., 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/1022">https://www.nii-kpssz.com/jour/article/view/1022</self-uri><abstract><sec><title>Основные положения</title><p>Основные положения</p></sec><sec><title> </title><p> </p></sec><sec><title>Цель</title><p>Цель. Оценить роль изменения длины теломерных участков хромосом при ишемической болезни сердца, обусловленной атеросклерозом коронарных артерий, в популяции жителей угледобывающего региона.</p></sec><sec><title>Материалы и методы</title><p>Материалы и методы. В исследование включены 60 пациентов с ишемической болезнью сердца (до операции и через пять лет после) и 52 здоровых человека. Выделение ДНК прoвoдили с использoванием стандартнoгo метoда фенoл-хлoрoфoрмнoй экстракции. Для измерения относительной длины теломер лейкоцитов использован метод количественной ПЦР. Анализ биохимических параметров выполнен стандартными методами. В качестве маркеров воспалительного процесса выбраны белки цитокины.</p></sec><sec><title>Результаты</title><p>Результаты. Теломеры у здоровых людей значимо длиннее, чем у пациентов с ишемической болезнью сердца. При этом длина теломерных участков ДНК не отличалась между пациентами до оперативного вмешательства и через 5 лет реабилитации. Для определения эффективности измерения теломер как маркера в патологии атеросклероза использован ROC-анализ. Площадь под ROC-кривой составила 0,998 ± 0,002. Обратная корреляционная зависимость выявлена между длиной теломер и общим содержанием Na, триглицеридов и липопротеинов высокой плотности. Значимая обратная корреляция между такими показателями липидного спектра, как триглицериды и липопротеины высокой плотности, выявлена только до оперативного вмешательства. Показана прямая и обратная зависимость длины теломер и интерлейкинов 33 и 10 соответственно.</p></sec><sec><title>Заключение</title><p>Заключение. Предположительно, воспалительные процессы и окислительные стресс, дополняя друг друга, являются причинами невосполнимых повреждений теломер, ускоряют процессы старения и приводят к необратимым последствиям в атерогенезе.</p></sec></abstract><trans-abstract xml:lang="en"><sec><title>Highlights</title><p>Highlights </p></sec><sec><title> </title><p> </p></sec><sec><title>Aim</title><p>Aim. To assess the impact of changes in the length of telomeric regions of chromosomes on the course of coronary artery disease caused by coronary artery atherosclerosis in the population of residents of a coal-mining region.</p></sec><sec><title>Methods</title><p>Methods. The study included 60 patients with coronary artery disease (before surgery and five years after) and 52 healthy participants. We isolated the DNA using the standard phenol-chloroform extraction method. We used the quantitative PCR method to measure the relative length of leukocyte telomeres and analyzed biochemical parameters using standard methods, selecting cytokine proteins as markers of the inflammatory process.</p></sec><sec><title>Results</title><p>Results. Telomeres in healthy participants were seven times longer compared to patients with coronary artery disease. At the same time, the length of telomeric regions of DNA did not differ in patients before surgery and after 5 years of rehabilitation. We used ROC analysis to determine the effectiveness of measuring telomeres as a marker of atherosclerosis. The area under the ROC curve was 0.998 ± 0.002. We found an inverse correlation between the telomere length and such parameters as the total body sodium, triglycerides and high-density lipoproteins. We noted a significant inverse correlation between such indicators of the lipid profile as triglycerides and high-density lipoproteins only in patients before surgery. The study results revealed direct and inverse dependence of the length of telomeres and cytokines such as IL-33 and IL-10, respectively.</p></sec><sec><title>Conclusion</title><p>Conclusion. Supposedly, inflammatory processes and oxidative stress, complementing each other, are the causes of irreparable damage to telomeres, accelerating the aging process and leading to irreversible consequences in atherogenesis.</p></sec></trans-abstract><kwd-group xml:lang="ru"><kwd>Длина теломер</kwd><kwd>Ишемическая болезнь сердца</kwd><kwd>Атеросклероз</kwd><kwd>ПЦР</kwd></kwd-group><kwd-group xml:lang="en"><kwd>Telomere length</kwd><kwd>Cardiac artery disease</kwd><kwd>Atherosclerosis</kwd><kwd>PCR</kwd></kwd-group><funding-group xml:lang="ru"><funding-statement>Исследование выполнено при поддержке комплексной программы фундаментальных научных исследований СО РАН в рамках фундаментальной темы НИИ КПССЗ № 0419-2022-0002 «Разработка инновационных моделей управления риском развития болезней системы кровообращения с учетом коморбидности на основе изучения фундаментальных, клинических, эпидемиологических механизмов и организационных технологий медицинской помощи в условиях промышленного региона Сибири».</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">Салахов Р.Р., Понасенко А.В. 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