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<article article-type="review-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">zabmedvestnik</journal-id><journal-title-group><journal-title xml:lang="ru">Забайкальский медицинский вестник</journal-title><trans-title-group xml:lang="en"><trans-title>Transbaikalian Medical Bulletin</trans-title></trans-title-group></journal-title-group><issn pub-type="epub">1998-6173</issn><publisher><publisher-name>Читинская государственная медицинская академия</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.52485/19986173_2026_2_139</article-id><article-id custom-type="elpub" pub-id-type="custom">zabmedvestnik-567</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>НАУЧНЫЕ ОБЗОРЫ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>SCIENTIFIC REVIEWS</subject></subj-group></article-categories><title-group><article-title>КАРДИОТОНИЧЕСКИЕ СТЕРОИДЫ КАК МОДУЛЯТОРЫ  СИГНАЛЬНЫХ ПУТЕЙ ВЫЖИВАНИЯ НЕЙРОНОВ:  ОБЗОР СОВРЕМЕННЫХ ИССЛЕДОВАНИЙ</article-title><trans-title-group xml:lang="en"><trans-title>CARDIOTONIC STEROIDS AS MODULATORS OF NEURONAL SURVIVAL SIGNALING PATHWAYS: A REVIEW OF CURRENT RESEARCH</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0009-0004-8357-441X</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Тепляшина</surname><given-names>Е. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Teplyashina</surname><given-names>E. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Тепляшина Елена Анатольевна, к.биол.н., доцент, доцент кафедры биологической химии с курсом медицинской, фармацевтической и токсикологической химии, старший научный сотрудник НИИ молекулярной медицины и патобиохимии </p><p>Researcher ID: AAN-8547-2020,Author ID Scopus: 56880351500. </p><p>660022, г. Красноярск, ул. Партизана Железняка, 1</p><p> </p></bio><bio xml:lang="en"><p>Elena A.Teplyashina, Candidate of Biological Sciences, Associate Professor, Associate Professor of the Department of Biological Chemistry with a course in Medical, Pharmaceutical and Toxicological Chemistry, Senior Researcher of the Research Institute of Molecular Medicine and Pathobiochemistry</p><p>Researcher ID: AAN-8547-2020, Author ID Scopus: 57202955297 </p><p>1 Partizana Zheleznyaka St., Krasnoyarsk, Russia, 660022</p></bio><email xlink:type="simple">elenateplyashina@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-3502-6388</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Шадрина</surname><given-names>Л. Б.</given-names></name><name name-style="western" xml:lang="en"><surname>Shadrina</surname><given-names>L. B.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Шадрина Людмила Борисовна, старший преподаватель кафедры биологической химии с курсом медицинской, фармацевтической и токсикологической химии, старший научный сотрудник НИИ молекулярной медицины и патобиохимии</p><p>Researcher ID: AAN-2127-2020, Author ID Scopus: 57202955297.</p><p>660022, г. Красноярск, ул. Партизана Железняка, 1</p><p> </p></bio><bio xml:lang="en"><p>Ludmila B. Shadrina, Senior Lecturer of the Department of Biological Chemistry with a course in Medical, Pharmaceutical and Toxicological Chemistry, Senior Researcher of the Research Institute of Molecular Medicine and Pathobiochemistry</p><p>Researcher ID: AAN-2127-2020, Author ID Scopus: 57202955297 </p><p>1 Partizana Zheleznyaka St., Krasnoyarsk, Russia, 660022</p><p> </p></bio><email xlink:type="simple">shaliu@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>ФГБОУ ВО «Красноярский государственный медицинский университет имени профессора В.Ф. Войно-Ясенецкого», Министерства здравоохранения РФ</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Prof. V.F. Voino-Yasenetsky Krasnoyarsk State Medical University</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2026</year></pub-date><pub-date pub-type="epub"><day>30</day><month>07</month><year>2026</year></pub-date><volume>0</volume><issue>2</issue><fpage>139</fpage><lpage>152</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Тепляшина Е.А., Шадрина Л.Б., 2026</copyright-statement><copyright-year>2026</copyright-year><copyright-holder xml:lang="ru">Тепляшина Е.А., Шадрина Л.Б.</copyright-holder><copyright-holder xml:lang="en">Teplyashina E.A., Shadrina L.B.</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://www.zabmedvestnik.ru/jour/article/view/567">https://www.zabmedvestnik.ru/jour/article/view/567</self-uri><abstract><p>Метаболизм клеток головного мозга характеризуется многочисленными клеточными и молекулярными механизмами. Воздействие повреждающих факторов на клетки головного мозга приводит к дисфункции митохондрий, накоплению активных форм кислорода и развитию окислительного стресса. Нейропротекция это совокупность механизмов направленных на защиту клеток центральной нервной системы. Эндогенные кардиотонические стероиды - уабаин и маринобуфагенин - обеспечивают замедление окислительных, биохимических и молекулярных сигнальных каскадов в нейронах головного мозга при воздействии на них стрессовых факторов. Цель настоящего обзора заключается в установлении новых представлений о механизмах действия кардиотонических стероидов на нейроны в физиологических и патофизиологических условиях.</p><p>Для изучения научных достижений в области взаимодействий Na+/K+-АТФазы и кардиотонических стероидов использовались такие методы как системно-структурный и сравнительный. Использование этих методов позволило представить авторскую схему, отображающую общие закономерности метаболических изменений Na+/K+-АТФазы при патологиях ЦНС. </p><p>На основе проанализированных литературных данных представлены молекулярные механизмы действия кардиотонических стероидов в физиологических и патологических условиях. Рассмотрены эндогенные и экзогенные представители класса кардиотонических стероидных метаболитов. Установлено, что действие этих гормоно-подобных соединений напрямую связано с Na+/K+-АТФазой, цитоплазматическими и мембранными белками. Выявлены потенциальные молекулярные формы кардиотонических стероидов, коррелирующие с развитием некоторых патофизиологических процессов в центральной нервной системе. </p><p>Сформулирован вывод о необходимости дальнейшего изучения механизма действия кардиотонических стероидных метаболитов как для фундаментальной нейробиологии, так и для клинической медицины.</p></abstract><trans-abstract xml:lang="en"><p>Brain cell metabolism is characterized by numerous cellular and molecular mechanisms. Exposure of brain cells to damaging factors leads to mitochondrial dysfunction, the accumulation of reactive oxygen species, and the development of oxidative stress. Neuroprotection is a set of mechanisms aimed at protecting cells of the central nervous system. Endogenous cardiotonic steroids – ouabain and marinobufagenin – slow down oxidative, biochemical, and molecular signaling cascades in brain neurons exposed to stress factors. </p><p>The aim of this review is to establish new understanding of the mechanisms of action of cardiotonic steroids on neurons under physiological and pathophysiological conditions. To study scientific advances in the interactions between Na+/K+-ATPase and cardiotonic steroids, methods such as systems-structural and comparative analysis were used. </p><p>Using these methods, we presented a schematic diagram depicting the general patterns of metabolic changes in Na+/K+-ATPase in CNS pathologies. Based on literature review, the molecular mechanisms of action of cardiotonic steroids under physiological and pathological conditions are presented. Endogenous and exogenous representatives of the class of cardiotonic steroid metabolites are examined. It is established that the action of these hormone-like compounds is directly linked to Na+/, K+-ATPase, cytoplasmic, and membrane proteins. Potential molecular forms of cardiotonic steroids that correlate with the development of certain pathophysiological processes in the central nervous system are identified. </p><p>A conclusion is drawn regarding the need for further study of the mechanism of action of cardiotonic steroid metabolites for both fundamental neurobiology and clinical medicine.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>метаболизм кардиотонических стероидов</kwd><kwd>уабаин</kwd><kwd>маринобуфагенин</kwd><kwd>дигоксин</kwd><kwd>Na+/K+-АТРаза</kwd><kwd>NF-κB</kwd><kwd>BDNF</kwd></kwd-group><kwd-group xml:lang="en"><kwd>metabolism of cardiotonic steroids</kwd><kwd>ouabain</kwd><kwd>marinobufagenin</kwd><kwd>digoxin</kwd><kwd>Na+/ K+-ATPase</kwd><kwd>NF-κB</kwd><kwd>BDNF</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">Lietzau G. Neurobiology Research on Neurodegenerative Disorders. 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