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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">bloodjour</journal-id><journal-title-group><journal-title xml:lang="ru">Гематология и трансфузиология</journal-title><trans-title-group xml:lang="en"><trans-title>Russian journal of hematology and transfusiology</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">0234-5730</issn><issn pub-type="epub">2411-3042</issn><publisher><publisher-name>ООО Издательский дом «Практика»</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.18821/0234-5730-2016-61-3-161-163</article-id><article-id custom-type="elpub" pub-id-type="custom">bloodjour-26</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 ЛИТЕРАТУРЫ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>REVIEWS OF LITERATURE</subject></subj-group></article-categories><title-group><article-title>Эритроферрон как эритроидный регулятор обмена железа</article-title><trans-title-group xml:lang="en"><trans-title>Erythroferrone as erythroid regulator of iron</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-1171-2746</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Будневский</surname><given-names>А. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Budnevskiy</surname><given-names>A. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>394000, г. Воронеж</p></bio><bio xml:lang="en"><p>Voronezh, 394000</p></bio><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-5212-1005</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Цветикова</surname><given-names>Л. Н.</given-names></name><name name-style="western" xml:lang="en"><surname>Tsvetikova</surname><given-names>L. N.</given-names></name></name-alternatives><bio xml:lang="ru"><p>394000, г. Воронеж</p></bio><bio xml:lang="en"><p>Voronezh, 394000</p></bio><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-5403-3356</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Воронина</surname><given-names>Е. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Voronina</surname><given-names>E. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>394000, г. Воронеж</p></bio><bio xml:lang="en"><p>Voronezh, 394000</p></bio><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-8545-6255</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Овсянников</surname><given-names>Е. С.</given-names></name><name name-style="western" xml:lang="en"><surname>Ovsyannikov</surname><given-names>E. S.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Овсянников Евгений Сергеевич, кандидат мед. наук, доцент кафедры факультетской терапии </p><p>394000, г. Воронеж</p></bio><bio xml:lang="en"><p>Ovsyannikov Evgeny S., MD, PhD, associate professor </p><p>Voronezh, 394000</p></bio><email xlink:type="simple">ovses@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/0000-0002-6809-9743</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Жусина</surname><given-names>Ю. Г.</given-names></name><name name-style="western" xml:lang="en"><surname>Zhusina</surname><given-names>Yu. G.</given-names></name></name-alternatives><bio xml:lang="ru"><p>394000, г. Воронеж</p></bio><bio xml:lang="en"><p>Voronezh, 394000</p></bio><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-9416-0010</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Лабжания</surname><given-names>Н. Б.</given-names></name><name name-style="western" xml:lang="en"><surname>Labzhaniya</surname><given-names>N. B.</given-names></name></name-alternatives><bio xml:lang="ru"><p>394000, г. Воронеж</p></bio><bio xml:lang="en"><p>Voronezh, 394000</p></bio><xref ref-type="aff" rid="aff-2"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>ГБОУ ВПО «Воронежский государственный медицинский университет им. Н.Н. Бурденко» Минздрава России</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Voronezh State Medical University named after N.N. Burdenko</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>ГБОУ ВПО «Воронежский государственный медицинский университет им. Н.Н. Бурденко» Минздрава России</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Voronezh State Medical University named after N.N. Burdenkо</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2016</year></pub-date><pub-date pub-type="epub"><day>27</day><month>02</month><year>2019</year></pub-date><volume>61</volume><issue>3</issue><fpage>161</fpage><lpage>163</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Будневский А.В., Цветикова Л.Н., Воронина Е.В., Овсянников Е.С., Жусина Ю.Г., Лабжания Н.Б., 2019</copyright-statement><copyright-year>2019</copyright-year><copyright-holder xml:lang="ru">Будневский А.В., Цветикова Л.Н., Воронина Е.В., Овсянников Е.С., Жусина Ю.Г., Лабжания Н.Б.</copyright-holder><copyright-holder xml:lang="en">Budnevskiy A.V., Tsvetikova L.N., Voronina E.V., Ovsyannikov E.S., Zhusina Y.G., Labzhaniya N.B.</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.htjournal.ru/jour/article/view/26">https://www.htjournal.ru/jour/article/view/26</self-uri><abstract><p>Железо является необходимым элементом жизнедеятельности клеток. Важнейшая роль железа определяется функциями белков, которые содержат этот биометалл: гемоглобин и миоглобин, осуществляющие транспортировку и накопление кислорода; ферменты, участвующие в процессах биологического окисления (цитохром р450); различные пероксидазы и каталазы, поддерживающие окислительно-восстановительный баланс организма. Метаболизм железа является уникальным процессом и регулируется целым рядом белков, обеспечивающих узкий безопасный диапазон содержания железа в клетках. Ключевым регулятором обмена железа на протяжении последних 10 лет считался 25-й-аминокислотный белок гепсидин. Гепсидин контролирует основные потоки распределения железа: абсорбция алиментарного железа в кишечнике, утилизация его макрофагами, фагоцитирующими старые эритроциты, и мобилизация железа из гепатоцитов. В литературе иногда встречался термин «эритроидный регулятор железа», однако долгое время нужный протеин оставался неуловимым. Предполагаемый эритроидный регулятор должен обеспечивать доставку железа в костный мозг за счет подавления экспрессии гепсидина в крови, тем самым увеличивая всасывание железа из энтероцитов и стимулируя высвобождение его из запасов. В недавних исследованиях были доказаны свойства мионектина как регулятора эритроидного железа. Впоследствии этот миокин был переименован в эритроферрон. В отличие от адаптивной роли, эритроферрон может способствовать перегрузке железом у больных тяжелыми наследственными анемиями, а также у пациентов, получавших частые гемотрансфузии. В данной статье мы представляем краткое обсуждение функции эритроферрона, а также рецепторов трансферрина 2 и их роль в обмене железа</p></abstract><trans-abstract xml:lang="en"><p>Iron is an essential element of the cell activity. The most important role of iron is determined by the functions of proteins that contain this metal: hemoglobin and myoglobin that execute the transport and storage of oxygen; enzymes involved in the processes of biological oxidation (cytochrome p450), various peroxidases and catalase supporting redox balance. Iron metabolism being unique process is regulated by a number of proteins, providing a narrow safe range of iron content in the cells. 25-amino acid protein hepcidin in the past 10 years was considered to be a key regulator of iron metabolism. Hepcidin controls main streams of the iron distribution: the absorption of nutritional iron in the intestine, utilization of its macrophages phagocyting old red blood cells, and iron mobilization from hepatocytes. In the literature there is occurred sometimes the term “erythroid regulator of iron metabolism”, however, for the long time the desired protein remained elusive. Proposed erythroid regulator should ensure the delivery of iron to the bone marrow due to suppression of blood expression of hepcidin, thereby increasing the absorption of iron from enterocytes and stimulating the release of its stock. In recent studies there were proved properties of myonectin as a regulator of erythroid iron. Subsequently, this myokine was renamed as erythroferrone. As distinct from the adaptive role erythroferrone may contribute to the iron overload in patients with severe hereditary anemias and in patients receiving frequent blood transfusions. In this paper, we present a brief discussion of functions of erythroferrones, as well as the transferrin receptor 2, and their role in iron metabolism.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>эритроферрон</kwd><kwd>гепсидин</kwd><kwd>обмен железа</kwd></kwd-group><kwd-group xml:lang="en"><kwd>erythroferrone</kwd><kwd>hepcidin</kwd><kwd>iron metabolism</kwd></kwd-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Lawen A., Lane D.J. Mammalian iron homeostasis in health and disease: uptake, storage, transport, and molecular mechanisms of action. Antioxid. Redox. Signal. 2013; 18(18): 2473—507.</mixed-citation><mixed-citation xml:lang="en">Lawen A., Lane D.J. Mammalian iron homeostasis in health and disease: uptake, storage, transport, and molecular mechanisms of action. Antioxid. Redox. 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