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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">urmj</journal-id><journal-title-group><journal-title xml:lang="ru">Уральский медицинский журнал</journal-title><trans-title-group xml:lang="en"><trans-title>Ural Medical Journal</trans-title></trans-title-group></journal-title-group><issn pub-type="epub">2949-4389</issn><publisher><publisher-name>Ural State Medical University</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.52420/2071-5943-2023-22-3-96-107</article-id><article-id custom-type="elpub" pub-id-type="custom">urmj-1275</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>Литературные обзоры | Literature reviews</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>Literature reviews</subject></subj-group></article-categories><title-group><article-title>Роль урокиназы, Т-кадгерина и адипонектина в развитии эндогенных депрессивных расстройств</article-title><trans-title-group xml:lang="en"><trans-title>The role of urokinase, T-cadherin and adiponetin in the development of endogenous depressive disorders</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-2903-4664</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Шелег</surname><given-names>Д. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Sheleg</surname><given-names>D. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Дмитрий Александрович Шелег – аспирант</p><p>Москва</p></bio><bio xml:lang="en"><p>Dmitrij A. Sheleg – Postgraduate student</p><p>Moscow</p></bio><email xlink:type="simple">sheleg-da@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/0000-0003-4289-3428</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Карагяур</surname><given-names>М. Н.</given-names></name><name name-style="western" xml:lang="en"><surname>Karagyaur</surname><given-names>M. N.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Максим Николаевич Карагяур – кандидат биологических наук</p><p>Москва</p></bio><bio xml:lang="en"><p>Maksim N. Karagyaur – Ph.D. in biology</p><p>Moscow</p></bio><email xlink:type="simple">m.karagyaur@mail.ru</email><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-1386-5922</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Примак</surname><given-names>А. Л.</given-names></name><name name-style="western" xml:lang="en"><surname>Primak</surname><given-names>A. L.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Александра Леонидовна Примак – лаборант-исследователь</p><p>Москва</p></bio><bio xml:lang="en"><p>Aleksandra L. Primak – Research Laboratory Assistant</p><p>Moscow</p></bio><email xlink:type="simple">primak.msu@mail.ru</email><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-2647-1284</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Нейфельд</surname><given-names>Е. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Neyfeld</surname><given-names>E. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Елена Арсланалиевна Нейфельд – кандидат медицинских наук</p><p>Москва</p></bio><bio xml:lang="en"><p>Elena A. Neyfeld – Ph.D. in medicine</p><p>Moscow</p></bio><email xlink:type="simple">ea.neyfeld@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Московский государственный медико-стоматологический университет им. А.И. Евдокимова</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Moscow State University of Medicine and Dentistry named after A.I. Evdokimov</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>Московский государственный университет им. М.В. Ломоносова</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Lomonosov Moscow State University</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2023</year></pub-date><pub-date pub-type="epub"><day>03</day><month>07</month><year>2023</year></pub-date><volume>22</volume><issue>3</issue><fpage>96</fpage><lpage>107</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Шелег Д.А., Карагяур М.Н., Примак А.Л., Нейфельд Е.А., 2023</copyright-statement><copyright-year>2023</copyright-year><copyright-holder xml:lang="ru">Шелег Д.А., Карагяур М.Н., Примак А.Л., Нейфельд Е.А.</copyright-holder><copyright-holder xml:lang="en">Sheleg D.A., Karagyaur M.N., Primak A.L., Neyfeld E.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://www.umjusmu.ru/jour/article/view/1275">https://www.umjusmu.ru/jour/article/view/1275</self-uri><abstract><sec><title>Введение</title><p>Введение. Распространенность депрессии в среднем составляет примерно 6 % от всего населения. Наследуемость депрессии составляет от 28 % до 44 %. Генетическая предрасположенность может быть обусловлена полиморфизмами генов, участвующих в процессах функционирования и морфогенеза головного мозга: балансе моноаминов, действии навигационных молекул и их рецепторов. </p><p>Цель работы – определить роль генов, регулирующих процессы миграции нервных клеток и направленного роста нервных волокон навигационных рецепторов (PLAUR и CDH13) или их лигандов (PLAU, PLAT, ADIPOQ) в развитии эндогенной депрессии и шизофрении в российской популяции.</p></sec><sec><title>Материалы и методы</title><p>Материалы и методы. На первом этапе исследования был выполнен поиск научной литературы в базе данных MedLine. Первичная распространенность геномных вариантов будет установлена с помощью полногеномного секвенирования 20 пациентов с тяжелыми формами шизофрении и эндогенной депрессии. Далее в исследовании примут участие не менее 100 пациентов в каждой группе и 100 человек здоровых доноров.</p></sec><sec><title>Результаты и обсуждение</title><p>Результаты и обсуждение. Рецептор урокиназы (uPAR) участвует в нейрогенезе, регулируя траекторию роста аксонов. Уровень suPAR в плазме крови может выступать в роли биомаркера слабовыраженного воспаления, лежащего в этиологии депрессии. Уровень suPAR в плазме можно считать прогностическим фактором эффективности сочетанной терапии антидепрессантами и противовоспалительными препаратами. Молекулы суперсемейства кадгеринов участвуют в развитии нервной системы, передаче межклеточных сигналов и регулировании пластичности нервных клеток. Полиморфизмы генов CDH7, CDH9, CDH13, CDH17 демонстрируют корреляцию с наличием депрессии. Адипонектин – гормон, выделяемый жировой тканью. Один из рецепторов адипонектина, AdipoR2, стимулирует нейронную пластичность, ингибирует воспаление и оксидативный стресс. У пациентов с депрессией концентрация адипонектина в плазме снижается.</p></sec><sec><title>Заключение</title><p>Заключение. Накопленные исследователями результаты свидетельствуют в пользу важной роли uPAR и Т-кадгерина в процессах развития головного мозга, а главное в патогенезе развития эндогенных депрессий.</p></sec></abstract><trans-abstract xml:lang="en"><p>Introduction The prevalence of depression averages approximately 6 % of the total population. The heritability of depression ranges from 28 % to 44 %. Genetic predisposition may be due to polymorphisms of genes involved in the processes of functioning and morphogenesis of the brain: the balance of monoamines, the action of navigational molecules and their receptors.</p><p>Purpose of the study To determine the role of genes that regulate the processes of nerve cell migration and directed growth of nerve fibers of navigation receptors (PLAUR and CDH13) or their ligands (PLAU, PLAT, ADIPOQ) in the development of endogenous depression and schizophrenia in the Russian population.</p><p>Materials and methods At the first stage of the study, the scientific literature was searched in the MEDLINE database. The primary prevalence of genomic variants will be established using whole genome sequencing of 20 patients with severe forms of schizophrenia and endogenous depression. Further, at least 100 patients in each group and 100 healthy donors will take part in the study.</p><p>Results and discussion The urokinase receptor (uPAR) is involved in neurogenesis by regulating the trajectory of axonal growth. The level of suPAR in blood plasma can act as a biomarker of mild inflammation underlying the etiology of depression. The level of suPAR in plasma can be considered a predictor of the effectiveness of combination therapy with antidepressants and anti-inflammatory drugs. Molecules of the cadherin superfamily are involved in the development of the nervous system, the transmission of intercellular signals, and the regulation of neuronal plasticity. Polymorphisms of the CDH7, CDH9, CDH13, CDH17 genes demonstrate a correlation with the presence of depression. Adiponectin is a hormone secreted by adipose tissue. One of the adiponectin receptors, AdipoR2, stimulates neuronal plasticity and inhibits inflammation and oxidative stress. Plasma concentrations of adiponectin are reduced in depressed patients.</p><p>Conclusion The results accumulated by researchers testify in favor of the important role of uPAR and T-cadherin in the processes of brain development, and most importantly, in the pathogenesis of the development of endogenous depressions.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>депрессия</kwd><kwd>урокиназа</kwd><kwd>т-кадгерин</kwd><kwd>адипонектин</kwd></kwd-group><kwd-group xml:lang="en"><kwd>depression</kwd><kwd>urokinase</kwd><kwd>t-cadherin</kwd><kwd>adiponectin</kwd></kwd-group><funding-group><funding-statement xml:lang="ru">Внешнее финансирование при проведении исследования отсутствовало.</funding-statement><funding-statement xml:lang="en">This study was not supported by any external sources of funding.</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">Malhi GS, Mann JJ. 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