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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="other" dtd-version="1.2" xml:lang="en"><front><journal-meta><journal-id journal-id-type="publisher-id">Morphology</journal-id><journal-title-group><journal-title xml:lang="en">Morphology</journal-title><trans-title-group xml:lang="ru"><trans-title>Морфология</trans-title></trans-title-group></journal-title-group><issn publication-format="print">1026-3543</issn><issn publication-format="electronic">2949-2556</issn><publisher><publisher-name xml:lang="en">Eco-Vector</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">698830</article-id><article-id pub-id-type="doi">10.17816/morph.698830</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>Научные обзоры</subject></subj-group><subj-group subj-group-type="article-type"><subject></subject></subj-group></article-categories><title-group><article-title xml:lang="en">ULTRASTRUCTURAL FEATURES OF PROGRAMMED CELL DEATH SPECIES: APOPTOSOME, INFLAMMASOME, AUTOPHAGOSOME</article-title><trans-title-group xml:lang="ru"><trans-title>УЛЬТРАСТРУКТУРНЫЕ ОСОБЕННОСТИ ПРОГРАММИРУЕМЫХ ВИДОВ КЛЕТОЧ-НОЙ ГИБЕЛИ: АПОПТОСОМА, ИНФЛАММАСОМА, АУТОФАГОСОМА</trans-title></trans-title-group><trans-title-group xml:lang="zh"><trans-title/></trans-title-group></title-group><contrib-group><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-3006-6281</contrib-id><contrib-id contrib-id-type="spin">4348-6781</contrib-id><name-alternatives><name xml:lang="en"><surname>Areshidze</surname><given-names>David</given-names></name><name xml:lang="ru"><surname>Арешидзе</surname><given-names>Давид Александрович</given-names></name><name xml:lang="zh"><surname></surname><given-names></given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="en"><p>MD, Cand. Sci. (Biology)</p>
<p>Head of Laboratory of Pathology of Cell</p></bio><bio xml:lang="ru"><p>Кандидат биологических наук</p>
<p>Заведующий лабораторией патологии клетки</p></bio><email>labcelpat@mail.ru</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-6251-2560</contrib-id><contrib-id contrib-id-type="spin">5647-1372</contrib-id><name-alternatives><name xml:lang="en"><surname>Kozlova</surname><given-names>Maria A</given-names></name><name xml:lang="ru"><surname>Козлова</surname><given-names>Мария Александровна</given-names></name><name xml:lang="zh"><surname></surname><given-names></given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="ru"><p>Старший научный сотрудник лаборатории патологии клетки, кандидат биологических наук</p></bio><email>kma-morph@mail.ru</email><xref ref-type="aff" rid="aff2"/></contrib></contrib-group><aff-alternatives id="aff1"><aff><institution xml:lang="en">Russian Scientific Center of Surgery named after academician B.V. Petrovsky</institution></aff><aff><institution xml:lang="ru">Российский научный центр хирургии имени академика Б.В. Петровского</institution></aff><aff><institution xml:lang="zh"></institution></aff></aff-alternatives><aff-alternatives id="aff2"><aff><institution xml:lang="en"></institution></aff><aff><institution xml:lang="ru">РНЦХ им.  Б.В. Петровского</institution></aff><aff><institution xml:lang="zh"></institution></aff></aff-alternatives><pub-date date-type="preprint" iso-8601-date="2026-08-21" publication-format="electronic"><day>21</day><month>08</month><year>2026</year></pub-date><volume>164</volume><issue>4</issue><issue-title xml:lang="ru"/><history><date date-type="received" iso-8601-date="2025-12-17"><day>17</day><month>12</month><year>2025</year></date><date date-type="accepted" iso-8601-date="2026-02-14"><day>14</day><month>02</month><year>2026</year></date></history><permissions><copyright-statement xml:lang="en">Copyright ©; , Eco-Vector</copyright-statement><copyright-statement xml:lang="ru">Copyright ©; , Эко-Вектор</copyright-statement><copyright-holder xml:lang="en">Eco-Vector</copyright-holder><copyright-holder xml:lang="ru">Эко-Вектор</copyright-holder><ali:free_to_read xmlns:ali="http://www.niso.org/schemas/ali/1.0/" start_date="2029-08-21"/><license><ali:license_ref xmlns:ali="http://www.niso.org/schemas/ali/1.0/">https://eco-vector.com/for_authors.php#07</ali:license_ref></license></permissions><self-uri xlink:href="https://j-morphology.com/1026-3543/article/view/698830">https://j-morphology.com/1026-3543/article/view/698830</self-uri><abstract xml:lang="en"><p>Cell death is a fundamental and physiologically necessary process in the development and functioning of a multicellular organism. Modern biology considers it not as chaotic necrosis, but as a set of strictly regulated programs, among which apoptosis, pyroptosis and autophagy are key. These processes are initiated by specific macromolecular complexes - apoptosome, inflammasome and autophagosome, respectively - whose unique ultrastructural organization directly determines their mechanism of action and biological consequences.</p> <p>This review systematizes current data on the morphology, composition, assembly dynamics and functional significance of these three complexes in the context of programmed cell death. The apoptosome forming the symmetric "spoke wheel" heptameric complex serves as a platform to activate caspase-9 and trigger "pure" apoptosis without inflammation. Inflammasome, which is a dynamic filamentous oligomer (ASC- "spot"), functions as a sensor of innate immunity, activating caspase-1 to process proinflammatory cytokines and induce pyroptosis - inflammatory cell death. The autophagosome, unlike protein oligomers, is a two-membrane vesicle mediating the degradation and recycling of intracellular components; under certain conditions, its hyperactivation can lead to autophagic cell death.</p> <p>A comparative analysis of the ultrastructural features of these complexes was carried out, a direct relationship was revealed between their specific architecture and the functions performed. A detailed study of their structure is not only fundamental to understanding the mechanisms of cell life and death, but also opens up prospects for the development of therapeutic strategies aimed at correcting disorders of the apoptosomal, inflammasomal and autophagic pathways in oncological, neurodegenerative, autoimmune and infectious diseases.</p></abstract><trans-abstract xml:lang="ru"><p>Клеточная гибель представляет собой фундаментальный и физиологически необходимый процесс в развитии и функционировании многоклеточного организма. Современная биология рассматривает ее не как хаотичный некроз, а как набор строго регулируемых программ, среди которых ключевое значение имеют апоптоз, пироптоз и аутофагия. Эти процессы инициируются специфическими макромолекулярными комплексами — апоптосомой, инфламмасомой и аутофагосомой соответственно, чья уникальная ультраструктурная организация напрямую определяет их механизм действия и биологические последствия.</p> <p>В данном обзоре систематизированы современные данные о морфологии, составе, динамике сборки и функциональном значении этих трех комплексов в контексте программируемой клеточной гибели. Апоптосома, формирующая симметричный гептамерный комплекс «колеса со спицами», служит платформой для активации каспазы-9 и запуска «чистого» апоптоза без воспаления. Инфламмасома, представляющая собой динамичный филаментозный олигомер (ASC-«пятно»), функционирует как сенсор врожденного иммунитета, активируя каспазу-1 для процессинга провоспалительных цитокинов и индукции пироптоза — воспалительной гибели клетки. Аутофагосома, в отличие от белковых олигомеров, является двухмембранной везикулой, опосредующей деградацию и рециклинг внутриклеточных компонентов; в определенных условиях ее гиперактивация может привести к аутофагической гибели клетки.</p> <p>Проведен сравнительный анализ ультраструктурных особенностей этих комплексов, выявлена прямая связь между их специфической архитектурой и выполняемыми функциями. Детальное изучение их строения имеет не только фундаментальное значение для понимания механизмов жизни и смерти клетки, но и открывает перспективы для разработки терапевтических стратегий, направленных на коррекцию нарушений апоптосомного, инфламмасомного и аутофагического путей при онкологических, нейродегенеративных, аутоиммунных и инфекционных заболеваниях.</p></trans-abstract><trans-abstract xml:lang="zh"><p/></trans-abstract><kwd-group xml:lang="en"><kwd>programmed cell death, apoptosis, pyroptosis, autophagy, ultrastructure, apoptosome, inflammasome, autophagosome, caspases, electron microcopy</kwd></kwd-group><kwd-group xml:lang="ru"><kwd>программируемая клеточная гибель, апоптоз, пироптоз, аутофагия, ультраструктура, апоптосома, инфламмасома, аутофагосома, каспазы, электронная микроскопия.</kwd></kwd-group><funding-group/></article-meta></front><body></body><back><ref-list><ref id="B1"><label>1.</label><citation-alternatives><mixed-citation xml:lang="en">1.	Deev R.V. 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