bmjourБайкальский медицинский журналBaikal Medical Journal2949-0715Irkutsk State Medical University10.57256/2949-0715-2025-4-2-12-21bmjour-289Research ArticleНаучные обзоры литературыScientific literature reviewsAP2A1 КАК НОВЫЙ РЕГУЛЯТОР КЛЕТОЧНОГО СТАРЕНИЯ: РОЛЬ В АДГЕЗИИ, ЦИТОСКЕЛЕТНОЙ ПЕРЕСТРОЙКЕ И ПЕРСПЕКТИВАХ ОМОЛОЖЕНИЯ КЛЕТОКAP2A1 AS A NOVEL REGULATOR OF CELLULAR AGING: ROLE IN ADHESION, CYTOSKELETAL REMODELING, AND PROSPECTS FOR CELL REJUVENATIONhttps://orcid.org/0000-0003-3285-5559ВоробьевВладимир АнатольевичVorobevVladimir A.

д.м.н., профессор кафедры факультетской хирургии и урологии;

 

Dr. Sci. (Med.), Professor of the Department of Faculty Surgery and Urology

terdenecer@gmail.comЩербатыхАндрей ВикторовичShcherbatykhAndrey V.

д.м.н., профессор, заведующий кафедрой факультетской хирургии и урологии; ректор

Dr. Sci. (Med.), Professor, Head of the Department of Faculty Surgery and Urology; rector

irkutskii@mail.ruhttps://orcid.org/0000-0002-3135-4616МаловСергей ИгоревичMalovSergey I.

д.м.н., профессор, проректор по научной работе

Dr. Sci. (Med.), Professor, Vice-Rector for Scientific Work

malovsergeii@mail.ruhttps://orcid.org/0000-0001-9278-9739ЛелявинКирилл БорисовичLelyavinKirill B.

д.м.н., доцент кафедры скорой медицинской помощи и медицины катастроф

Dr. Sci. (Med.), Associate Professor of the Department of Emergency Medical Care and Disaster Medicine

lelyavinK@rambler.ruhttps://orcid.org/0000-0003-1525-3425ТухиевАртур РуслановичTukhievArtur R.

аспирант кафедры факультетской хирургии и урологии

Graduate Student of the Department of Faculty Surgery and Urology

atukhiev@bk.ruИркутский государственный медицинский университет, ИркутскРоссияIrkutsk State Medical UniversityRussian FederationИркутский государственный медицинский университет, ИрктускРоссияIrkutsk State Medical UniversityRussian FederationРоссийская медицинская академия непрерывного профессионального образования, ИркутскРоссияIrkutsk State Medical Academy of Postgraduate Education - branch of the Russian Medical Academy of Postgraduate EducationRussian Federation202510062025421221Copyright © Воробьев В.А., Щербатых А.В., Малов С.И., Лелявин К.Б., Тухиев А.Р., 20252025Воробьев В.А., Щербатых А.В., Малов С.И., Лелявин К.Б., Тухиев А.Р.Vorobev V.A., Shcherbatykh A.V., Malov S.I., Lelyavin K.B., Tukhiev A.R.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.bmjour.ru/jour/article/view/289Актуальность

Актуальность. Старение клеток – один из ключевых факторов возраст-ассоциированных заболеваний, и понимание его механизмов открывает возможности для разработки антивозрастных стратегий. Недавние исследования показали, что белок AP2A1 (Adaptor Protein 2 Alpha 1 subunit), ранее известный как участник эндоцитоза, играет важную роль в поддержании сенесцентного фенотипа клеток. В стареющих клетках AP2A1 локализуется вдоль актиновых стресс-волокон, взаимодействует с интегрином β1 и способствует укреплению адгезии клеток к внеклеточному матриксу. Эти изменения позволяют сенесцентным клеткам поддерживать увеличенный размер и блокировать пролиферацию. Экспериментально показано, что подавление AP2A1 приводит к частичному омоложению клеток – уменьшению их размеров, снижению уровней маркеров сенесценции (p53, p21, SA-β-gal) и ослаблению адгезии [1]. Напротив, повышение экспрессии AP2A1 в молодых клетках индуцирует ускоренное старение. Эти данные демонстрируют, что AP2A1 – не только маркер старения, но и активный регулятор клеточного состояния. Потенциально, AP2A1 может стать мишенью для антивозрастных мероприятий, направленных на модификацию адгезивных свойств сенесцентных клеток, ослабление их влияния на ткани и возможное обратимое омоложение.

Заключение

Заключение. В данной статье проводится систематический обзор литературы по роли AP2A1 в механизмах клеточного старения, его связи с интегриновыми путями и перспективам его модуляции в целях биомедицины.

Relevance

Relevance. Cellular aging is a major contributor to age-related diseases, and understanding its mechanisms opens avenues for anti-aging strategies.

The aim of this review is to systematically analyze the literature data on the role of the AP2A1 protein in the processes of cellular aging and rejuvenation.

Results

Results. Recent studies have identified AP2A1 (Adaptor Protein 2 Alpha 1 subunit), previously known for its role in endocytosis, as a crucial regulator of the senescent cell phenotype. In aged cells, AP2A1 localizes along actin stress fibers, interacts with integrin β1, and promotes strong adhesion to the extracellular matrix. These changes allow senescent cells to maintain their enlarged size and sustain cell cycle arrest. Experimental data show that AP2A1 knockdown leads to partial rejuvenation, characterized by reduced cell size, decreased senescence markers (p53, p21, SA-β-gal), and weakened adhesion. Conversely, AP2A1 overexpression in young cells accelerates senescence. These findings suggest that AP2A1 is not merely a biomarker of aging but an active regulator of cellular state. Targeting AP2A1 could offer a novel anti-aging therapeutic approach, aiming to modify senescent cell adhesion properties, mitigate their impact on tissues, and potentially induce partial rejuvenation.

Conclusion

Conclusion: This review provides a systematic analysis of AP2A1’s role in cellular aging, its link to integrin pathways, and the therapeutic potential of its modulation in biomedicine.

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The authors declare that there are no conflicts of interest present.