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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">cfpd</journal-id><journal-title-group><journal-title xml:lang="ru">Бюллетень физиологии и патологии дыхания</journal-title><trans-title-group xml:lang="en"><trans-title>Bulletin Physiology and Pathology of Respiration</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1998-5029</issn><publisher><publisher-name>Дальневосточный научный центр физиологии и патологии дыхания</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.36604/1998-5029-2025-97-137-151</article-id><article-id custom-type="elpub" pub-id-type="custom">cfpd-1280</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>ОБЗОРЫ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>REVIEWS</subject></subj-group></article-categories><title-group><article-title>Рецепторы горького вкуса TAS2R как перспективные мишени в персонализированной терапии бронхиальной астмы</article-title><trans-title-group xml:lang="en"><trans-title>Bitter taste receptors TAS2R as promising targets in personalised therapy of asthma</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>Конев</surname><given-names>А. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Konev</surname><given-names>A. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Андрей Викторович Конев, аспирант, младший научный сотрудник, лаборатория механизмов вирус-ассоциированных патологий развития</p><p>675000, г. Благовещенск, ул. Калинина, 22</p></bio><bio xml:lang="en"><p>Andrey V. Konev, Postgraduate student, Junior Staff Scientist, Laboratory of Mechanisms of Virus-Associated Developmental Pathology of Respiration</p><p>22 Kalinina Str., Blagoveshchensk, 675000</p></bio><email xlink:type="simple">andrkonev@vk.com</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Федеральное государственное бюджетное научное учреждение «Дальневосточный научный центр физиологии и патологии дыхания»</institution></aff><aff xml:lang="en"><institution>Far Eastern Scientific Center of Physiology and Pathology of Re</institution></aff></aff-alternatives><pub-date pub-type="collection"><year>2025</year></pub-date><pub-date pub-type="epub"><day>21</day><month>09</month><year>2025</year></pub-date><volume>0</volume><issue>97</issue><fpage>137</fpage><lpage>151</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Конев А.В., 2025</copyright-statement><copyright-year>2025</copyright-year><copyright-holder xml:lang="ru">Конев А.В.</copyright-holder><copyright-holder xml:lang="en">Konev A.V.</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://cfpd.elpub.ru/jour/article/view/1280">https://cfpd.elpub.ru/jour/article/view/1280</self-uri><abstract><p>В обзоре обобщены современные данные о роли эктопических рецепторов горького вкуса (TAS2R) в патогенезе бронхиальной астмы (БА) в контексте персонализированного подхода к терапии. TAS2R, экспрессируемые в эпителии дыхательных путей, гладкой мускулатуре и иммунокомпетентных клетках, участвуют в ключевых звеньях воспалительного процесса и регуляции бронхиального тонуса. Активация TAS2R приводит к релаксации гладкой мускулатуры дыхательных путей через сигнальные каскады, независимые от β2-адренорецепторов и цАМФ, что обеспечивает эффективность в условиях сниженной чувствительности к β2-агонистам. В Т2-высоком эндотипе БА TAS2R подавляют интерлейкины (ИЛ)-4, ИЛ-5, ИЛ-13, снижая эозинофильное воспаление и дегрануляцию тучных клеток. В не-Т2-вариантах БА рецепторы ингибируют провоспалительные медиаторы (ИЛ-17, ИЛ-8, фактора некроза опухоли α), уменьшают активность нейтрофилов и макрофагов. TAS2R рассматриваются как перспективные фармакологические мишени, особенно в трудно контролируемых формах астмы, резистентных к ингаляционным глюкокортикостероидам. В научной литературе упоминаются исследования препаратов, которые обладают агонистической активностью в отношении TAS2R, и ведутся поиски эндогенных агонистов рецепторов. Представленный материал подчёркивает необходимость дальнейших исследований, направленных на уточнение молекулярных механизмов действия TAS2R, перспективы применения TAS2R-ориентированной терапии при различных эндотипах БА, оценку клинической эффективности и безопасности терапевтических агентов, направленных на персонализацию лечения БА на основе изучения генетических и функциональных особенностей этих рецепторов.</p></abstract><trans-abstract xml:lang="en"><p>This review summarises current data on the role of ectopic bitter-taste receptors (TAS2R) in the pathogenesis of asthma within a personalised-therapy framework. TAS2R expressed in airway epithelium, airway smoothmuscle cells and immunocompetent cells participate in key inflammatory pathways and regulate bronchial tone. Receptor activation induces airway smooth-muscle relaxation through signalling cascades that are independent of β2-adrenergic receptors and cAMP, maintaining efficacy when β2-agonist sensitivity is reduced. In the T2-high endotype, TAS2R suppress IL-4, IL-5 and IL-13, thereby attenuating eosinophilic inflammation and mast-cell degranulation. In non-T2 asthma, TAS2R inhibit pro-inflammatory mediators (IL-17, IL-8/CXCL8, TNF-α) and curb neutrophil and macrophage activity. Consequently, TAS2R are viewed as promising pharmacological targets, particularly for difficult-to-control asthma resistant to inhaled glucocorticosteroids. The literature already cites compounds with TAS2R-agonist activity, and the search for novel endogenous agonists is ongoing. The evidence underscores the need for further studies to clarify TAS2R molecular mechanisms, evaluate TAS2R-oriented therapy across asthma endotypes, and assess the clinical efficacy and safety of agents designed to personalise treatment based on the genetic and functional characteristics of these receptors.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>TAS2R</kwd><kwd>бронхиальная астма</kwd><kwd>гладкомышечные клетки дыхательных путей</kwd><kwd>иммуномодуляция</kwd><kwd>эпителиальный барьер</kwd><kwd>цитокины</kwd><kwd>персонализированная терапия</kwd></kwd-group><kwd-group xml:lang="en"><kwd>TAS2R</kwd><kwd>asthma</kwd><kwd>airway smooth-muscle cells</kwd><kwd>immunomodulation</kwd><kwd>epithelial barrier</kwd><kwd>cytokines</kwd><kwd>personalised therapy</kwd></kwd-group><funding-group><funding-statement xml:lang="ru">Исследование выполнено при поддержке Российского научного фонда (проект No23-15-00372)</funding-statement><funding-statement xml:lang="en">This study was supported by Russian Science Foundation (project No23-15-00372)</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">Global initiative for asthma (GINA). 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