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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">10.36604/1998-5029-2026-99-134-149</article-id><article-id custom-type="elpub" pub-id-type="custom">cfpd-1323</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>Анкириновый ионный канал и нейротрофический фактор мозга в патогенезе бронхиальной астмы: пути взаимодействий</article-title><trans-title-group xml:lang="en"><trans-title>Transient receptor potential ankyrin channel and brain-derived neurotrophic factor in the pathogenesis of asthma: ways of interaction</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-5018-0271</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Кытикова</surname><given-names>О. Ю.</given-names></name><name name-style="western" xml:lang="en"><surname>Kytikova</surname><given-names>O. Yu.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Оксана Юрьевна Кытикова, д-р мед. наук, научный сотрудник</p><p>лаборатория восстановительного лечения</p><p>690105; ул. Русская, 73г; Владивосток</p></bio><bio xml:lang="en"><p>Oxana Yu. Kytikova, MD, PhD, DSc (Med.), Staff Scientist</p><p>Laboratory of Rehabilitative Treatment</p><p>690105; 73g Russkaya Str.; Vladivostok</p></bio><email xlink:type="simple">kytikova@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/0000-0002-6058-201X</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Новгородцева</surname><given-names>Т. П.</given-names></name><name name-style="western" xml:lang="en"><surname>Novgorodtseva</surname><given-names>T. P.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Татьяна Павловна Новгородцева, д-р биол. наук, профессор, зам. директора по научной работе, главный научный сотрудник</p><p>лаборатория биомедицинских исследований</p><p>690105; ул. Русская, 73г; Владивосток</p></bio><bio xml:lang="en"><p>Tatiana P. Novgorodtseva, PhD, DSc (Biol.), Рrofessor, Deputy Director on Scientific Work, Main Staff Scientist</p><p>Laboratory of Biomedical Research</p><p>690105; 73g Russkaya Str.; Vladivostok</p></bio><email xlink:type="simple">nauka@niivl.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/0000-0002-2492-3198</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Антонюк</surname><given-names>М. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Antonyuk</surname><given-names>M. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Марина Владимировна Антонюк, д-р мед. наук, профессор, зав. лабораторией</p><p>лаборатория восстановительного лечения</p><p>690105; ул. Русская, 73г; Владивосток</p></bio><bio xml:lang="en"><p>Marina V. Antonyuk, MD, PhD, DSc (Med.), Рrofessor, Head of Laboratory</p><p>Laboratory of Rehabilitative Treatment</p><p>690105; 73g Russkaya Str.; Vladivostok</p></bio><email xlink:type="simple">antonyukm@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/0000-0002-6413-9840</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Гвозденко</surname><given-names>Т. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Gvozdenko</surname><given-names>T. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Татьяна Александровна Гвозденко, д-р мед. наук, профессор РАН,главный научный сотрудник, директор</p><p>лаборатория восстановительного лечения</p><p>690105; ул. Русская, 73г; Владивосток</p></bio><bio xml:lang="en"><p>Tatiana A. Gvozdenko, MD, PhD, DSc (Med.), Professor of RAS, Main Staff Scientist, Director</p><p>Laboratory of Rehabilitative Treatment</p><p>690105; 73g Russkaya Str.; Vladivostok</p></bio><email xlink:type="simple">vfdnz@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Владивостокский филиал Федерального государственного бюджетного научного учреждения «Дальневосточный научный центр физиологии и патологии дыхания» – Научно-исследовательский институт медицинской климатологии и восстановительного лечения</institution></aff><aff xml:lang="en"><institution>Vladivostok Branch of Far Eastern Scientific Center of Physiology and Pathology of Respiration – Research Institute of Medical Climatology and Rehabilitative Treatment</institution></aff></aff-alternatives><pub-date pub-type="collection"><year>2026</year></pub-date><pub-date pub-type="epub"><day>30</day><month>03</month><year>2026</year></pub-date><volume>0</volume><issue>99</issue><fpage>134</fpage><lpage>149</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Кытикова О.Ю., Новгородцева Т.П., Антонюк М.В., Гвозденко Т.А., 2026</copyright-statement><copyright-year>2026</copyright-year><copyright-holder xml:lang="ru">Кытикова О.Ю., Новгородцева Т.П., Антонюк М.В., Гвозденко Т.А.</copyright-holder><copyright-holder xml:lang="en">Kytikova O.Y., Novgorodtseva T.P., Antonyuk M.V., Gvozdenko T.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://cfpd.elpub.ru/jour/article/view/1323">https://cfpd.elpub.ru/jour/article/view/1323</self-uri><abstract><p>   Сложность патогенеза бронхиальной астмы (БА) обусловлена влиянием факторов окружающей среды, генетических и эпигенетических факторов, взаимодействующих между собой и способствующих развитию и обострениям данной патологии. БА имеет нейрогенный компонент, к которому в последние годы приковано внимание исследователей. При действии холода, сигаретного дыма, аллергенов и ряда химических веществ, являющихся триггерами БА, активируется экспрессируемый в сенсорных С-волокнах легких анкириновый рецептор TRPA1 (от англ. transient receptor potential cation channel subfamily A member 1). Он запускает приток Са2+ в сенсорные нейроны и активирует каскады, ответственные за экспрессию гена нейротрофического фактора мозга (от англ. brain-derived neurotrophic factor, BDNF). BDNF вовлечен в развитие ремоделирования дыхательных путей, усиливает иннервацию бронхов и усугубляет их гиперреактивность, в также поддерживает гиперчувствительность нейронов по механизму обратной связи. Полиморфизмы гена BDNF определяют восприимчивость к развитию БА, при этом носители полиморфизмов гена TRPА1 более чувствительны к эпигенетическим модификациям и могут иметь более сильную экспрессию BDNF в ответ на действие раздражителей. Несмотря на то, что эпигенетика TRPА1 и BDNF при БА находится в стадии изучения, эпигенетические изменения TRPА1 и BDNF достаточно хорошо описаны в неврологии, что может быть интересно в контексте их взаимовлияния при БА, учитывая роль нейроиммунного воспаления в патогенезе данного заболевания. В настоящем обзоре обсуждаются роль и взаимосвязь генетических и эпигенетических изменений, вызванных факторами окружающей среды, инициирующих развитие БА, а также место TRPА1 и BDNF в данном процессе.</p></abstract><trans-abstract xml:lang="en"><p>   The complexity of the pathogenesis of bronchial asthma (BA) has been caused by the influence of the environmental, genetic and epigenetic factors that interact with each other and contribute to the development and exacerbation of this pathology. In recent years researchers have focused on the neurogenic component of the BA pathogenesis. The ankyrin receptor TRPA1(the transient receptor potential cation channel subfamily A member 1) is expressed in the sensory C-fibers of the lungs and activated by the cold, cigarette smoke, allergens and number of chemicals that are the triggers of BA. It triggers the influx of Ca2+ into sensory neurons and activates the cascades responsible for the expression of the brain-derived neurotrophic factor (BDNF) gene. BDNF is involved in airway remodeling, enhances airway innervation and exacerbates airway hyperreactivity, and also maintains sensory hypersensitivity through a feedback loop. BDNF gene polymorphisms confer susceptibility to BA, with carriers of TRPA1 gene polymorphisms more sensitive to epigenetic modifications and may have strong BDNF expression in response to the stimuli. Despite the fact that the epigenetics of TRPA1 and BDNF in BA is under study, the epigenetic changes of TRPA1 and BDNF are well described in neurology, which may be interesting in the context of their interaction in BA, given the role of neuroimmune inflammation in the pathogenesis of this disease. The present review discusses the role and relationship of genetic and epigenetic changes induced by environmental factors initiating BA development, as well as role of TRPA1 and BDNF in this process.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>бронхиальная астма</kwd><kwd>генетика</kwd><kwd>эпигенетика</kwd><kwd>BDNF</kwd><kwd>TRP-каналы</kwd><kwd>TRPA1</kwd><kwd>нейрогенное воспаление</kwd></kwd-group><kwd-group xml:lang="en"><kwd>asthma</kwd><kwd>genetic</kwd><kwd>epigenetic</kwd><kwd>BDNF</kwd><kwd>TRP channels</kwd><kwd>TRPA1</kwd><kwd>neurogenic inflammation</kwd></kwd-group><funding-group><funding-statement xml:lang="ru">Исследование проводилось без участия спонсоров</funding-statement><funding-statement xml:lang="en">This study was not sponsored</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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