russjcardiolРоссийский кардиологический журналRussian Journal of Cardiology1560-40712618-7620«SILICEA-POLIGRAF» LLC10.15829/1560-4071-2025-6058DKFMPFrussjcardiol-6058Research ArticleОБЗОРЫ ЛИТЕРАТУРЫREVIEWИнфламмасома — новый взгляд на терапию сердечно-сосудистых заболеваний. Часть IIInflammasome — a new look at the therapy of cardiovascular diseases. Part IIhttps://orcid.org/0000-0002-8493-5211РубинштейнА. А.RubinsteinA. A.

Лаборант-исследователь НИЛ аутоиммунных и аутовоспалительных заболеваний НЦМУ.

Санкт-Петербург

St. Petersburg

cardiojournal@yandex.ruhttps://orcid.org/0000-0002-9391-5546ХодотА. А.KhodotA. A.

Лаборант кафедры Факультетской терапии с клиникой.

Санкт-Петербург

St. Petersburg

https://orcid.org/0000-0002-4433-1640ТириковаП. В.TirikovaP. V.

Лаборант-исследователь НИЛ аутоиммунных и аутовоспалительных заболеваний НИЦ неизвестных, редких и генетически обусловленных заболеваний НЦМУ ЦПМ.

Санкт-Петербург

St. Petersburg

https://orcid.org/0000-0002-7577-628XГоловкинА. С.GolovkinA. S.

д. м. н., в. н. с., руководитель группы генно-клеточной инженерии институт молекулярной биологии и генетики; в. н. с. НИЛ аутоиммунных и аутовоспалительных заболеваний НЦМУ.

Санкт-Петербург

St. Petersburg

https://orcid.org/0000-0001-7204-7850КудрявцевИ. В.KudryavtsevI. V.

к. б. н., доцент, зав. лабораторией НИЛ аутоиммунных и аутовоспалительных заболеваний НЦМУ; зав. лабораторией клеточной иммунологии, ФГБНУ Институт экспериментальной медицины РАН.

Санкт-Петербург

St. Petersburg

https://orcid.org/0000-0003-2929-0980ШляхтоЕ. В.ShlyakhtoE. V.

д. м. н., профессор, академик РАН, генеральный директор.

Санкт-Петербург

St. Petersburg

ФГБУ НМИЦ им. В.А. Алмазова Минздрава РоссииРоссияAlmazov National Medical Research CenterRussian Federation202506052025306SОбзоры литературы, мнения по проблеме60586058Copyright © Рубинштейн А.А., Ходот А.А., Тирикова П.В., Головкин А.С., Кудрявцев И.В., Шляхто Е.В., 20252025Рубинштейн А.А., Ходот А.А., Тирикова П.В., Головкин А.С., Кудрявцев И.В., Шляхто Е.В.Rubinstein A.A., Khodot A.A., Tirikova P.V., Golovkin A.S., Kudryavtsev I.V., Shlyakhto E.V.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://russjcardiol.elpub.ru/jour/article/view/6058

Роль инфламмасом при сердечно-сосудистых заболеваниях в настоящее время изучена недостаточно, однако есть некоторое количество исследований последних лет, показывающих участие этих мультибелковых комплексов в развитии и прогрессировании сердечно-сосудистых заболеваний. Так, при фибрилляции предсердий запуск инфламмасомы способствует уменьшению длительности и рефрактерности предсердного потенциала действия, индукции ранней и/или отсроченной постдеполяризации, что поддерживает эктопическую активность. При хронической сердечной недостаточности запуск инфламмасомного каскада инициирует и поддерживает хроническое воспаление, приводящее к ремоделированию сердечной ткани и развитию фиброза. В ишемической болезни сердца активация инфламмасомы способствует поддержанию ишемии и увеличению области очагов некроза. Воспалительные реакции при перикардитах и миокардитах также не обходятся без участия этого мультибелкового комплекса. При данных патологиях ингибирование инфламмасомы способствует улучшению клинической симптоматики и нормализации функциональной способности сердечной ткани. Таким образом, при вышеперечисленных заболеваниях использование препаратов-ингибиторов инфламмасом может стать достаточно перспективным методом терапии.

The role of inflammasomes in cardiovascular diseases has not been sufficiently studied at present. However, there are a number of recent studies showing the participation of these multiprotein complexes in the development and progression of cardiovascular diseases. Thus, in atrial fibrillation, the inflam­masome triggering helps to reduce the duration and refractivity of the atrial action potential, induction of early and/or delayed afterdepolarization, which maintains ectopic activity. In heart failure, the triggering of inflammasome cascade initiates and maintains chronic inflammation, leading to cardiac remo­deling and fibrosis. In coronary artery disease, inflammasome activation maintains ischemia and increases the necrosis area. Inflammatory reactions in pericarditis and myocarditis also do not occur without the participation of this multiprotein complex. In these pathologies, inflammasome inhibition helps to improve clinical symptoms and normalize the cardiac function. Therefore, inflammasome inhibitor agents can become a promising method of therapy in the above diseases.

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