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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">arthyper</journal-id><journal-title-group><journal-title xml:lang="ru">Артериальная гипертензия</journal-title><trans-title-group xml:lang="en"><trans-title>"Arterial’naya Gipertenziya" ("Arterial Hypertension")</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1607-419X</issn><issn pub-type="epub">2411-8524</issn><publisher><publisher-name>Antihypertensive League</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.18705/1607-419X-2024-2359</article-id><article-id custom-type="edn" pub-id-type="custom">DXUNEA</article-id><article-id custom-type="elpub" pub-id-type="custom">arthyper-2359</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>Статьи</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>Articles</subject></subj-group></article-categories><title-group><article-title>Роль кишечной микробиоты в развитии артериальной гипертензии: механизмы и терапевтические мишени</article-title><trans-title-group xml:lang="en"><trans-title>The role of intestinal microbiota in the development of arterial hypertension: mechanisms and therapeutic targets</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-3096-9747</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Борщев</surname><given-names>Ю. Ю.</given-names></name><name name-style="western" xml:lang="en"><surname>Borshchev</surname><given-names>Yu. Yu.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Борщев Юрий Юрьевич — кандидат биологических наук, ведущий научный сотрудник, заведующий научно-исследовательским отделом токсикологии </p><p>Санкт-Петербург</p></bio><bio xml:lang="en"><p>Yury Yu. Borshchev, PhD in Biological Sciences, Leading Researcher, Department of Toxicology</p><p>St Petersburg</p></bio><email xlink:type="simple">borshchev_yuyu@almazovcentre.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/0000-0003-1705-7217</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Сонин</surname><given-names>Д. Л.</given-names></name><name name-style="western" xml:lang="en"><surname>Sonin</surname><given-names>D. L.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Сонин Дмитрий Леонидович — кандидат медицинских наук, ведущий научный сотрудник, руководитель научно-исследовательского отдела микроциркуляции и метаболизма миокарда </p><p>Санкт-Петербург</p></bio><bio xml:lang="en"><p>Dmitry L. Sonin, MD, PhD, Leading Researcher, Research Department of Microcirculation and Myocardial Metabolism</p><p>St Petersburg</p></bio><email xlink:type="simple">sonin_dl@almazovcentre.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/0000-0001-6382-5286</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Минасян</surname><given-names>С. М.</given-names></name><name name-style="western" xml:lang="en"><surname>Minasian</surname><given-names>S. M.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Минасян Саркис Минасович — кандидат медицинских наук, ведущий научный сотрудник</p><p>Санкт-Петербург</p></bio><bio xml:lang="en"><p>Sarkis M. Minasian, MD, PhD, Senior Researcher, Research Department of Microcirculation and Myocardial Metabolism</p><p>St Petersburg</p></bio><email xlink:type="simple">carkis@yandex.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/0000-0002-9217-9890</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Процак</surname><given-names>Е. С.</given-names></name><name name-style="western" xml:lang="en"><surname>Protsak</surname><given-names>E. S.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Процак Егор Сергеевич — младший научный сотрудник научно-исследовательского отдела токсикологии</p><p>Санкт-Петербург</p></bio><bio xml:lang="en"><p>Egor S. Protsak,   MD,   Junior   Researcher,   Department of Toxicology</p><p>St Petersburg</p></bio><email xlink:type="simple">egor-protsak@yandex.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/0000-0003-4069-0678</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Семенова</surname><given-names>Н. Ю.</given-names></name><name name-style="western" xml:lang="en"><surname>Semenova</surname><given-names>N. Yu.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Семенова Наталья Юрьевна — кандидат биологических наук, старший научный сотрудник научно-исследовательского отдела патоморфологии </p><p>Санкт-Петербург</p></bio><bio xml:lang="en"><p>Natalia Yu. Semenova, PhD in Biological Sciences, Senior Researcher, Department of Patomorphology</p><p>St Petersburg</p></bio><email xlink:type="simple">semenova_nyu@almazovcentre.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/0000-0001-5129-9944</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Галагудза</surname><given-names>М. М.</given-names></name><name name-style="western" xml:lang="en"><surname>Galagudza</surname><given-names>M. M.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Галагудза Михаил Михайлович — доктор медицинских наук, профессор, член-корреспондент РАН, главный научный сотрудник научно-исследовательского отдела микроциркуляции и метаболизма миокарда, директор Института экспериментальной медицины </p><p>ул. Аккуратова, д. 2, Санкт-Петербург, 197341</p></bio><bio xml:lang="en"><p>Mikhail M. Galagudza, MD, DSc, Professor, Corresponding Member of the Russian Academy of Sciences, Chief Researcher, Research Department of Microcirculation and Myocardial Metabolism, Director of the Institute of Experimental Medicine</p><p>2 Akkuratov str., St Petersburg, 197341</p></bio><email xlink:type="simple">galagudza_mm@almazovcentre.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Федеральное государственное бюджетное учреждение «Национальный медицинский исследовательский центр имени В. А. Алмазова» Министерства здравоохранения Российской Федерации</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Almazov National Medical Research Centre</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2024</year></pub-date><pub-date pub-type="epub"><day>07</day><month>11</month><year>2023</year></pub-date><volume>30</volume><issue>2</issue><fpage>159</fpage><lpage>173</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Борщев Ю.Ю., Сонин Д.Л., Минасян С.М., Процак Е.С., Семенова Н.Ю., Галагудза М.М., 2024</copyright-statement><copyright-year>2024</copyright-year><copyright-holder xml:lang="ru">Борщев Ю.Ю., Сонин Д.Л., Минасян С.М., Процак Е.С., Семенова Н.Ю., Галагудза М.М.</copyright-holder><copyright-holder xml:lang="en">Borshchev Y.Y., Sonin D.L., Minasian S.M., Protsak E.S., Semenova N.Y., Galagudza M.M.</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://htn.almazovcentre.ru/jour/article/view/2359">https://htn.almazovcentre.ru/jour/article/view/2359</self-uri><abstract><p>Кишечная микробиота не только опосредует влияние на организм ряда факторов риска сердечно-сосудистых заболеваний, но и может играть активную роль в регуляции артериального давления (АД) за счет изменения проницаемости кишечного эпителиального барьера и продукции вазоактивных метаболитов. При этом изучение молекулярных механизмов, лежащих в основе влияния кишечной микробиоты на уровень АД, находится на начальном этапе. В обзоре проведен анализ научной литературы, посвященной роли кишечной микробиоты в развитии артериальной гипертензии (АГ), описаны ключевые механизмы прогипертензивного действия метаболитов кишечной микробиоты и представлены данные о новых подходах к лечению АГ, основанных на воздействии на состав и функцию кишечной микрофлоры. На уровень АД влияют молекулы, концентрация которых в крови прямо или опосредованно связана с активностью кишечной микрофлоры. Эти биоактивные молекулы могут быть разделены на две группы — образующиеся клетками иммунной системы человека в результате стимуляции со стороны микробиоты и образующиеся ферментативным путем в результате метаболической активности самой микробиоты. К первой группе относятся молекулярные механизмы, связанные с активацией иммунитета и системной воспалительной реакцией, а ко второй — короткоцепочечные жирные кислоты, триметиламин-N-оксид, желчные кислоты, уремические токсины и биогенные амины. АГ сопровождается специфическими изменениями состава кишечной микробиоты, причем в последние годы исследователями установлены причинно-следственные отношения между определенными энтеротипами и развитием АГ. Более того, сформировавшаяся АГ сама по себе является причиной изменений профиля кишечного микробиома. Более глубокое понимание молекулярных механизмов, опосредующих влияние микробиоты на АД, может послужить основой для разработки новых подходов к лечению АГ.</p></abstract><trans-abstract xml:lang="en"><p>The intestinal microbiota not only mediates the influence of a number of risk factors for cardiovascular diseases on the body, but can also play an active role in the regulation of blood pressure (BP) by changing the permeability of the intestinal epithelial barrier and the production of vasoactive metabolites. At the same time, the study of the molecular mechanisms underlying the influence of intestinal microbiota on BP levels is at an early stage. The review analyzes the scientific literature on the role of intestinal microbiota in the development of arterial hypertension (HTN), describes the key mechanisms of the prohypertensive action of intestinal microbiota metabolites, and presents data on new approaches to the treatment of HTN based on effects on the composition and function of intestinal microflora. BP levels are affected by molecules whose concentration in the blood is directly or indirectly related to the activity of intestinal microflora. These bioactive molecules can be divided into two groups — those formed by cells of the human immune system as a result of stimulation by the microbiota and those formed enzymatically as a result of the metabolic activity of the microbiota itself. The first group includes molecular mechanisms associated with immune activation and systemic inflammatory response, and the second group includes short-chain fatty acids, trimethylamine-N-oxide, bile acids, uremic toxins and biogenic amines. HTN is accompanied by specific changes in the composition of the intestinal microbiota, and in recent years, researchers have established cause-and-effect relationships between certain enterotypes and the development of HTN. Moreover, established HTN itself causes changes in the intestinal microbiome profile. A deeper understanding of the molecular mechanisms mediating the influence of microbiota on BP may serve as the basis for the development of new approaches to the treatment of HTN.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>кишечная микробиота</kwd><kwd>пробиотики</kwd><kwd>артериальное давление</kwd><kwd>артериальная гипертензия</kwd><kwd>системное воспаление</kwd><kwd>короткоцепочечные жирные кислоты</kwd></kwd-group><kwd-group xml:lang="en"><kwd>intestinal microbiota</kwd><kwd>probiotics</kwd><kwd>blood pressure</kwd><kwd>hypertension</kwd><kwd>systemic inflammation</kwd><kwd>shortchain fatty acids</kwd></kwd-group><funding-group><funding-statement xml:lang="ru">Исследование выполнено за счет гранта Российского научного фонда (проект № 23-15-00139, https://rscf.ru/project/23-15-00139/)</funding-statement><funding-statement xml:lang="en">The research was carried out at the expense of a grant from the Russian Science Foundation (project No. 23-15-00139, https://rscf.ru/project/23-15-00139 /)</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">Юдина Ю. 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