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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">transmed</journal-id><journal-title-group><journal-title xml:lang="ru">Трансляционная медицина</journal-title><trans-title-group xml:lang="en"><trans-title>Translational Medicine</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2311-4495</issn><issn pub-type="epub">2410-5155</issn><publisher><publisher-name>Almazov National Medical Research Centre, Saint Petersburg, Russia</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.18705/2311-4495-2016-3-6-21-31</article-id><article-id custom-type="elpub" pub-id-type="custom">transmed-269</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>НЕВРОЛОГИЯ И НЕЙРОХИРУРГИЯ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>NEUROLOGY AND NEUROSURGERY</subject></subj-group></article-categories><title-group><article-title>ВОССТАНОВИТЕЛЬНЫЙ ПОСТИШЕМИЧЕСКИЙ НЕЙРОГЕНЕЗ: ПЕРСПЕКТИВЫ КЛИНИЧЕСКОГО ПРИМЕНЕНИЯ</article-title><trans-title-group xml:lang="en"><trans-title>NEUROGENESIS AFTER CEREBRAL ISCHEMIA: CLINICAL APPLICATION PROSPECTS</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>Ходанович</surname><given-names>М. Ю.</given-names></name><name name-style="western" xml:lang="en"><surname>Khodanovich</surname><given-names>M. Yu.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Ходанович Марина Юрьевна - доктор биологических наук, профессор, Томский государственный университет.</p><p>Пр. Ленина, д. 36, Томск, 634050</p></bio><bio xml:lang="en"><p>Marina  Yu.  Khodanovich - Dr.  Sc.,  professor.</p><p>Lenina pr., 36 Tomsk, 634050</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>Кисель</surname><given-names>А. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Kisel</surname><given-names>A. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Кисель Алена Андреевна - аспирант.</p><p>Пр. Ленина, д. 36, Томск, 634050, e-mail: kisell.alena@gmail.com</p></bio><bio xml:lang="en"><p>Alena A. Kisel - PhD-student.</p><p>Lenina pr., 36 Tomsk, 634050, e-mail: kisell.alena@gmail.com</p></bio><email xlink:type="simple">kisell.alena@gmail.com</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Национальный исследовательский Томский государственный университет</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Tomsk State University</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2016</year></pub-date><pub-date pub-type="epub"><day>05</day><month>04</month><year>2017</year></pub-date><volume>3</volume><issue>6</issue><fpage>21</fpage><lpage>31</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Ходанович М.Ю., Кисель А.А., 2017</copyright-statement><copyright-year>2017</copyright-year><copyright-holder xml:lang="ru">Ходанович М.Ю., Кисель А.А.</copyright-holder><copyright-holder xml:lang="en">Khodanovich M.Y., Kisel A.A.</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://transmed.almazovcentre.ru/jour/article/view/269">https://transmed.almazovcentre.ru/jour/article/view/269</self-uri><abstract><p>В настоящее время существует два основных подхода к изучению восстановления мозга после ишемического инсульта. Один из них связан с введением стволовых клеток в повреждённый мозг. Другой подход направлен на стимуляцию эндогенных процессов восстановления, в частности, постнатального нейрогенеза. Настоящий обзор рассматривает изменения постнатального нейрогенеза, вызванные ишемией мозга, и возможные пути регуляции этого процесса. Множество исследований на моделях животных демонстрируют, что нейрогенез в основном усиливается после ишемии, однако, несмотря на усиленную пролиферацию и миграцию нейрональных предшественников к зоне инсульта, большинство новых нейронов погибает, так и не созрев. Кроме того, усиление нейрогенеза в патологическом состоянии происходит в основном за счёт рекрутинга новых стволовых клеток, а не за счёт дополнительных делений клеток-предшественниц, что приводит, в конечном итоге, к ещё большему снижению способности к регенерации. Таким образом, эндогенных репаративных механизмов недостаточно, и необходим поиск новых мишеней для активизации пролиферации, выживания и созревания новых нейронов после ишемического инсульта. В качестве потенциальных регуляторов постишемического нейрогенеза рассматриваются ростовые факторы, системы нейротрансмиттеров и противовоспалительные препараты, а также показанное в последнее время перепрограммирование астроцитов в нейроны.</p></abstract><trans-abstract xml:lang="en"><p>Today two main approaches are in the focus of neurobiological studies of brain recovery after a stroke. The first is concerned with the infusion of stem cells in damaged brain. The second approach is directed at the stimulation of endogenous reparative processes, in particular, adult neurogenesis. This review considers alterations of adult neurogenesis caused by cerebral ischemia and possible pathways of its regulation. Numerous studies performed on animals have shown that adult neurogenesis is mostly increased after cerebral ischemia. Increased proliferation of neural stem cells and migration of newborn cells towards to infarct zone make adult neurogenesis a potential target for brain recovery. However, the most part of newborn neurons die before reaching maturity. Besides, an increase of neurogenesis in pathological conditions is mainly due to recruitment of new stem cells, but not due to an additional precursor-cells division that results in an overall decline of the regeneration capacity. Thus, the endogenous reparative mechanisms are not sufficient, and the search for new targets to promote proliferation, survival, and maturation of new neurons after a stroke is needed. Neurotransmitter systems, growth factors, and anti-inflammatory drugs are considered as potential regulators of post-ischemic neurogenesis. Besides, recent studies showed direct reprogramming of astcrocytes to neurons after brain damage.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>ишемия мозга</kwd><kwd>инсульт</kwd><kwd>постнатальный нейрогенез</kwd><kwd>нейрональные стволовые клетки</kwd><kwd>модели на животных</kwd></kwd-group><kwd-group xml:lang="en"><kwd>cerebral ischemia</kwd><kwd>stroke</kwd><kwd>adult neurogenesis</kwd><kwd>neural stem cells</kwd><kwd>animal model</kwd></kwd-group><funding-group><funding-statement xml:lang="ru">РНФ</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">10 ведущих причин смерти в мире: информ. бюл. ВОЗ № 310. Всемирная организация здравоохранения. http://www.who.int/mediacentre/factsheets/fs310/ru/ (4.10.2016).</mixed-citation><mixed-citation xml:lang="en">10 ведущих причин смерти в мире: информ. бюл. ВОЗ № 310. 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