spbmedicalrecordsНовые Санкт-Петербургские врачебные ведомостиNew St. Petersburg Medical Records1609-2201Первый Санкт-Петербургский государственный медицинский университет имени академика И.П. Павлова10.24884/1609-2201-2026-105-1-19-43spbmedicalrecords-124Research ArticleОБЗОРЫ ЛИТЕРАТУРЫLITERATURE REVIEWSРоль эффекторов врожденного иммунитета в патогенезе острого коронарного синдрома, хронического коронарного синдрома и постинфарктного кардиофиброзаThe role of innate immunity effectors in the pathogenesis of acute coronary syndrome, chronic coronary syndrome and post-infarction cardiac fibrosishttps://orcid.org/0000-0002-7196-6166ДюсеновД. О.DyusenovD. O.

Дюсенов Даурен Оразбаевич, аспирант

Санкт-Петербург

Dauren O. Dyusenov, Postgraduate Student

Saint Petersburg

dauren.dyusenov@inbox.ruhttps://orcid.org/0000-0002-4625-2671ФроловД. С.FrolovD. S.

Фролов Дмитрий Сергеевич, кандидат медицинских наук, доцент кафедры терапии госпитальной с курсом аллергологии и иммунологии имени ак. М. В. Черноруцкого с клиникой; доцент кафедры пропедевтики внутренних болезней

Санкт-Петербург

 

Dmitriy S. Frolov, Cand. of Sci. (Med.), Associate Professor of the Department of Hospital Therapy with a course in Allergology and Immunology named after M. V. Chernorutsky with a clinic; Associate Professor of the Department of Propaedeutics of Internal Diseases

Saint Petersburg

froloff_82@mail.ruhttps://orcid.org/0000-0002-4433-1640ТириковаП. В.TirikovaP. V.

Тирикова Полина Валерьевна, лаборант-исследователь НИЛ аутоиммунных и аутовоспалительных заболеваний НИЦ неизвестных, редких и генетически обусловленных заболеваний НЦМУ «Центр персонализированной медицины»

Санкт-Петербург

Polina V. Tirikova, Research Laboratory Assistant, Research Laboratory of Autoimmune and Autoinflammatory Diseases

Saint Petersburg

tipo.paulina2002@yandex.ruhttps://orcid.org/0009-0003-2376-3246ЛитвиноваД. Д.LitvinovaD. D.

Литвинова Диана Даниловна, студент

Санкт-Петербург

Diana D. Litvinova, Student

Saint Petersburg

litvinova.diana.danilovna@mail.ruhttps://orcid.org/0000-0002-8493-5211РубинштейнА. А.RubinsteinA. A.

Рубинштейн Артем Аркадьевич, младший научный сотрудник

Санкт-Петербург

Artem A. Rubinstein, Junior Research Fellow

Saint Petersburg

arrubin6@mail.ruhttps://orcid.org/0000-0001-7204-7850КудрявцевИ. В.KudryavtsevI. V.

Кудрявцев Игорь Владимирович, кандидат биологических наук, доцент, заведующий лабораторией клеточной иммунологии

Санкт-Петербург

Igor V. Kudryavtsev, Cand. of Sci. (Biol.), Associate Professor, Head of the Laboratory of Cellular Immunology

Saint Petersburg

igorek1981@yandex.ruhttps://orcid.org/0000-0002-2440-7222МарченкоВ. Н.MarchenkoV. N.

Марченко Валерий Николаевич, доктор медицинских наук, профессор кафедры госпитальной терапии с курсом аллергологии и иммунологии им. акад. М. В. Черноруцкого с клиникой

Санкт-Петербург

Valeriy N. Marchenko, Dr. of Sci. (Med.), Professor, Department of Hospital Therapy with the Course of Allergology and Immunology named after Acad. M. V. Chernorutskiy

Saint Petersburg

marchvn@mail.ruПервый Санкт-Петербургский государственный медицинский университет имени академика И. П. ПавловаРоссияPavlov UniversityRussian FederationПервый Санкт-Петербургский государственный медицинский университет имени академика И. П. Павлова; Санкт-Петербургский государственный университетРоссияPavlov University; St. Petersburg State UniversityRussian FederationНациональный медицинский исследовательский центр имени В. А. АлмазоваРоссияAlmazov National Medical Research CentreRussian FederationСеверо-Западный государственный медицинский университет имени И. И. МечниковаРоссияI. I. Mechnikov, North-Western State MedicalRussian FederationИнститут экспериментальной медициныРоссияInstitute of Experimental MedicineRussian Federation202608072026011943Copyright © Дюсенов Д.О., Фролов Д.С., Тирикова П.В., Литвинова Д.Д., Рубинштейн А.А., Кудрявцев И.В., Марченко В.Н., 20262026Дюсенов Д.О., Фролов Д.С., Тирикова П.В., Литвинова Д.Д., Рубинштейн А.А., Кудрявцев И.В., Марченко В.Н.Dyusenov D.O., Frolov D.S., Tirikova P.V., Litvinova D.D., Rubinstein A.A., Kudryavtsev I.V., Marchenko V.N.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.docved.ru/jour/article/view/124

В литературном обзоре представлено современное состояние проблемы участия эффекторных клеток врожденного иммунитета в патогенезе ишемической болезни сердца (ИБС) и ее осложнений. Концепция атеросклероза как воспалительного заболевания получила убедительное подтверждение в клинических исследованиях CANTOS, COLCOT и LoDoCo2, продемонстрировавших снижение частоты сердечно-сосудистых событий при таргетном подавлении ключевых звеньев воспалительного каскада. Вместе с тем крупнейшее исследование CLEAR SYNERGY, набор участников которого в значительной мере проходил в условиях пандемии COVID-19, не выявило снижения частоты сердечно-сосудистых событий при назначении колхицина в острой фазе инфаркта миокарда, несмотря на достоверное снижение активности воспалительного процесса, подтвержденное лабораторными маркерами системного воспаления, что свидетельствует о необходимости дальнейшего уточнения оптимального временного окна назначения противовоспалительной терапии в острой фазе инфаркта миокарда. В отличие от существующих обзоров, рассматривающих отдельные клеточные популяции, настоящая работа систематизирует данные о молекулярных механизмах воспаления (инфламмасомы NLRP3 и AIM2) и ключевых клеточных эффекторах врожденного иммунитета — моноцитах и макрофагах, нейтрофилах, тучных клетках, базофилах, эозинофилах и естественных киллерах (NK-клетках) — в единую фазоспецифическую модель на основе исключительно клинических данных, полученных в исследованиях с участием человека. Проанализированы результаты исследований при остром коронарном синдроме (ОКС), хроническом коронарном синдроме (ХКС), постинфарктном кардиосклерозе и декомпенсации хронической сердечной недостаточности (ХСН). Показано, что инфламмасомный каскад NLRP3/каспаза-1/ интерлейкин-1β/интерлейкин-18 выступает в роли ключевого медиатора сигналов от кристаллов холестерина, окисленных липопротеинов низкой плотности и молекулярных паттернов повреждения. Представлены данные о прогностическом значении субпопуляционного состава моноцитов (CD14++CD16−, CD14++CD16+, CD14+CD16++) и поляризации макрофагов (М1/М2) в атеросклеротической бляшке. Рассмотрена роль нейтрофильных внеклеточных ловушек (NETs) в формировании коронарного тромба и дестабилизации бляшки. Охарактеризовано участие тучных клеток и базофилов в процессах ишемии-реперфузии и тканевого ремоделирования, а также значение NK-клеток в атеротромбозе и постинфарктном воспалении. Установленная фазоспецифичность вклада отдельных клеточных популяций врожденного иммунитета открывает перспективы для разработки персонализированных противовоспалительных стратегий у пациентов с различными клиническими формами ИБС.

Atherosclerosis is increasingly recognised as an inflammatory disease. The concept of residual inflammatory risk has been confirmed in the CANTOS, COLCOT, and LoDoCo2 trials, which demonstrated a reduction in cardiovascular events through targeted suppression of key inflammatory pathways. However, the largest trial of colchicine in acute myocardial infarction — CLEAR SYNERGY — conducted predominantly during the COVID-19 pandemic, did not demonstrate a reduction in cardiovascular events despite significant suppression of systemic inflammatory markers, underscoring the need for further clarification of the optimal therapeutic window and conditions for anti-inflammatory interventions. Unlike existing reviews that typically address individual innate immune cell populations in isolation, the present review systematically integrates key innate immune effectors — inflammasomes (NLRP3, AIM2), monocytes and macrophages, neutrophils, mast cells, basophils, eosinophils, and natural killer (NK) cells — into a unified phase-specific model based exclusively on human clinical data.

A literature search was performed using PubMed, Scopus, and Web of Science databases. Original research articles and systematic reviews/meta-analyses from Q1/Q2 peer-reviewed journals were included. Only human studies or in vitro studies using human-derived material were eligible; animal model studies were excluded.

The NLRP3/caspase-1/interleukin-1β/interleukin-18 inflammasome cascade functions as a central integrator of signals from cholesterol crystals, oxidised low-density lipoproteins, and damage-associated molecular patterns. Intermediate monocytes (CD14++CD16+) independently predict cardiovascular events. M1-macrophage predominance in plaque shoulder regions is associated with instability, while M2-macrophages facilitate efferocytosis and repair. Neutrophil extracellular traps (NETs) provide a prothrombotic scaffold in coronary thrombi, with citrullinated histone H3 and myeloperoxidase-DNA complexes correlating with infarct size. Mast cell density predicts adverse cardiovascular outcomes, whereas basophils and eosinophils demonstrate phase-dependent protective or detrimental roles. NK cell cytotoxic activity is systemically reduced in coronary artery disease, while CD56bright NK cells selectively accumulate in unstable plaques.

The phase-specific contribution of individual innate immune cell populations — from chronic inflammation through plaque destabilisation, post-infarction remodelling, and heart failure decompensation — provides a rationale for the development of personalised anti-inflammatory strategies in patients with various clinical manifestations of coronary artery disease.

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