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<article 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" xmlns:ali="http://www.niso.org/schemas/ali/1.0/" article-type="research-article" dtd-version="1.2" xml:lang="en"><front><journal-meta><journal-id journal-id-type="publisher-id">Acta Naturae</journal-id><journal-title-group><journal-title xml:lang="en">Acta Naturae</journal-title><trans-title-group xml:lang="ru"><trans-title>Acta Naturae</trans-title></trans-title-group></journal-title-group><issn publication-format="print">2075-8251</issn><publisher><publisher-name xml:lang="en">Acta Naturae Ltd</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">10350</article-id><article-id pub-id-type="doi">10.32607/20758251-2018-10-1-4-14</article-id><article-categories><subj-group subj-group-type="toc-heading" xml:lang="en"><subject>Reviews</subject></subj-group><subj-group subj-group-type="toc-heading" xml:lang="ru"><subject>Обзоры</subject></subj-group><subj-group subj-group-type="article-type"><subject>Research Article</subject></subj-group></article-categories><title-group><article-title xml:lang="en">“Social Life” of Senescent Cells: What Is SASP and Why Study It?</article-title><trans-title-group xml:lang="ru"><trans-title>«Социальная жизнь» стареющих клеток: что такое SASP и зачем его изучать?</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Borodkina</surname><given-names>A. V.</given-names></name><name xml:lang="ru"><surname>Бородкина</surname><given-names>А. В.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><email>borodkina618@gmail.com</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Deryabin</surname><given-names>P. I.</given-names></name><name xml:lang="ru"><surname>Дерябин</surname><given-names>П. И.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><email>borodkina618@gmail.com</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Giukova</surname><given-names>А. А.</given-names></name><name xml:lang="ru"><surname>Грюкова</surname><given-names>А. А.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><email>borodkina618@gmail.com</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Nikolsky</surname><given-names>N. N.</given-names></name><name xml:lang="ru"><surname>Никольский</surname><given-names>Н. Н.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><email>borodkina618@gmail.com</email><xref ref-type="aff" rid="aff1"/></contrib></contrib-group><aff-alternatives id="aff1"><aff><institution xml:lang="en">Institute of Cytology, Russian Academy of Sciences</institution></aff><aff><institution xml:lang="ru">Институт цитологии РАН</institution></aff></aff-alternatives><pub-date date-type="pub" iso-8601-date="2018-03-15" publication-format="electronic"><day>15</day><month>03</month><year>2018</year></pub-date><volume>10</volume><issue>1</issue><issue-title xml:lang="en">VOL 10, NO1 (2018)</issue-title><issue-title xml:lang="ru">ТОМ 10, №1 (2018)</issue-title><fpage>4</fpage><lpage>14</lpage><history><date date-type="received" iso-8601-date="2020-01-17"><day>17</day><month>01</month><year>2020</year></date></history><permissions><copyright-statement xml:lang="en">Copyright ©; 2018, Borodkina A.V., Deryabin P.I., Giukova А.А., Nikolsky N.N.</copyright-statement><copyright-statement xml:lang="ru">Copyright ©; 2018, Бородкина А.В., Дерябин П.И., Грюкова А.А., Никольский Н.Н.</copyright-statement><copyright-year>2018</copyright-year><copyright-holder xml:lang="en">Borodkina A.V., Deryabin P.I., Giukova А.А., Nikolsky N.N.</copyright-holder><copyright-holder xml:lang="ru">Бородкина А.В., Дерябин П.И., Грюкова А.А., Никольский Н.Н.</copyright-holder><ali:free_to_read xmlns:ali="http://www.niso.org/schemas/ali/1.0/"/><license><ali:license_ref xmlns:ali="http://www.niso.org/schemas/ali/1.0/">https://creativecommons.org/licenses/by/4.0</ali:license_ref></license></permissions><self-uri xlink:href="https://actanaturae.ru/2075-8251/article/view/10350">https://actanaturae.ru/2075-8251/article/view/10350</self-uri><abstract xml:lang="en"><p>Cellular senescence was first described as a failure of normal human cells to divide indefinitely in culture. Until recently, the emphasis in the study of cell senescence has been focused on the accompanying intracellular processes. The focus of the attention has been on the irreversible growth arrest and two important physiological functions that rely on it: suppression of carcinogenesis due to the proliferation loss of damaged cells, and the acceleration of organism aging due to the deterioration of the tissue repair mechanism with age. However, the advances of the past years have revealed that senescent cells can impact the surrounding tissue microenvironment, and, thus, that the main consequences of senescence are not solely mediated by intracellular alterations. Recent studies have provided evidence that a pool of molecules secreted by senescent cells, including cytokines, chemokines, proteases and growth factors, termed the senescence-associated secretory phenotype (SASP), via autocrine/paracrine pathways can affect neighboring cells. Today it is clear that SASP functionally links cell senescence to various biological processes, such as tissue regeneration and remodeling, embryonic development, inflammation, and tumorigenesis. The present article aims to describe the “social” life of senescent cells: basically, SASP constitution, molecular mechanisms of its regulation, and its functional role.</p></abstract><trans-abstract xml:lang="ru"><p>Феномен клеточного старения впервые был описан как предел деления нормальных клеток в культуре. С момента первого упоминания и вплоть до недавнего времени основной акцент при изучении клеточного старения был сделан на внутриклеточных изменениях, сопровождающих этот процесс. Наибольшее внимание уделялось необратимой остановке пролиферации стареющих клеток и двум логично вытекающим физиологическим следствиям - супрессии канцерогенеза за счет ареста роста поврежденных клеток и ускорению организменного старения ввиду ухудшения репарации тканей с возрастом. Однако в настоящее время наблюдается смещение акцентов при исследовании клеточного старения. Оказалось, что стареющие клетки через ауто/паракринный механизм могут влиять на клетки микроокружения, секретируя множество различных факторов, включая цитокины, хемокины, протеазы и ростовые факторы. Такой профиль секретируемых стареющими клетками молекул получил название ассоциированного со старением секреторного фенотипа (senescence associated secretory phenotype, SASP). На сегодняшний день известно, что SASP опосредует участие стареющих клеток в самых разнообразных биологических процессах, включая регенерацию, ремоделирование тканей, эмбриогенез, воспаление и туморогенез. Настоящий обзор посвящен описанию «социальной жизни» стареющих клеток, а именно: составу, механизмам регуляции и функциональной роли ассоциированного со старением секреторного фенотипа.</p></trans-abstract><kwd-group xml:lang="en"><kwd>antagonistic pleiotropy</kwd><kwd>cellular senescence</kwd><kwd>immune clearance</kwd><kwd>senescence-associated secretory phenotype</kwd><kwd>stem cells</kwd><kwd>tumor suppression</kwd><kwd>tumorigenesis</kwd></kwd-group><kwd-group xml:lang="ru"><kwd>антагонистическая плейотропия</kwd><kwd>ассоциированный со старением секреторный фенотип</kwd><kwd>иммунный клиренс</kwd><kwd>клеточное старение</kwd><kwd>стволовые клетки</kwd><kwd>супрессия опухолей</kwd><kwd>туморогенез</kwd></kwd-group><funding-group><funding-statement xml:lang="en">This work was supported by the Russian Science Foundation (Project No. 14-50-00068).</funding-statement><funding-statement xml:lang="ru">Работа выполнена при финансовой поддержке Российского научного фонда (проект № 14-50-00068).</funding-statement></funding-group></article-meta></front><body></body><back><ref-list><ref id="B1"><label>1.</label><mixed-citation>[1] Carrel A. // J. 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