russjcardiolРоссийский кардиологический журналRussian Journal of Cardiology1560-40712618-7620«SILICEA-POLIGRAF» LLC10.15829/1560-4071-2019-2-92-98russjcardiol-2894Research ArticleОБЗОРЫ ЛИТЕРАТУРЫREVIEWАнализ транскриптома макрофагов при атерогенезеAnalysis of macrophage transcriptome in atherogenesishttps://orcid.org/0000-0002-8834-1111КубекинаМ. В.KubekinaM. V.

Кубекина Марина Владиславовна — аспирант, младший научный сотрудник; SPIN-код: 2156-2430

Moscow

marykumy@gmail.comhttps://orcid.org/0000-0002-2082-2429НикифоровН. Г.NikiforovN. G.

Никифоров Никита Геннадьевич  — младший научный сотрудник

Moscow

nikiforov.mipt@googlemail.comhttps://orcid.org/0000-0003-0501-8499КарагодинВ. П.KaragodinV. P.

Карагодин Василий Петрович — доктор биологических наук, профессор кафедры товароведения и товарной экспертизы

Moscow

vpka@mail.ruhttps://orcid.org/0000-0003-0978-6444СобенинИ. А.SobeninI. A.

Собенин Игорь Александрович — доктор биологических наук, главный научный сотрудниклаборатории медицинской генетики

Moscow

igor.sobenin@gmail.comhttps://orcid.org/0000-0002-6495-1628ОреховА. Н.OrekhovA. N.

Орехов Александр Николаевич — доктор биологических наук, заведующийлаборатории клеточных механизмов атерогенеза

Moscow; Skolkovo

a.h.opexob@gmail.comИнститут биологии гена Российской академии наук; ФГБНУ Научно-исследовательский институт общей патологии и патофизиологииРоссияInstitute of Gene Biology; The Institute of General Pathology and PathophysiologyRussian FederationИнститут биологии гена Российской академии наук; ФГБУ Национальный медицинский исследовательский центр кардиологии Минздрава России; ФГБНУ Научно-исследовательский институт общей патологии и патофизиологииРоссияInstitute of Gene Biology; National Medical Research Center of Cardiology; The Institute of General Pathology and PathophysiologyRussian FederationРоссийский экономический университет им. Г.В. ПлехановаРоссияPlekhanov Russian University of EconomicsRussian FederationФГБУ Национальный медицинский исследовательский центр кардиологии Минздрава РоссииРоссияNational Medical Research Center of CardiologyRussian FederationФГБНУ Научно-исследовательский институт общей патологии и патофизиологии; Научно-исследовательский институт атеросклероза, Инновационный центр СколковоРоссияThe Institute of General Pathology and Pathophysiology; Scientific Institute of Atherosclerosis ResearchRussian Federation201907032019029298Copyright © Кубекина М.В., Никифоров Н.Г., Карагодин В.П., Собенин И.А., Орехов А.Н., 20192019Кубекина М.В., Никифоров Н.Г., Карагодин В.П., Собенин И.А., Орехов А.Н.Kubekina M.V., Nikiforov N.G., Karagodin V.P., Sobenin I.A., Orekhov A.N.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/2894

Накопление холестерина под влиянием модифицированных липопротеидов низкой плотности является ключевым событием атерогенеза. Известно, что атеросклероз сопровождается хроническим локальным воспалением. Моноциты/макрофаги, ключевые клетки врожденного иммунитета, способны не только захватывать и накапливать липиды в сосудистой стенке, но и секретировать сигнальные молекулы, влияющие на функции других клеток. Для атеросклеротического поражения характерна неспособность благополучно завершить воспалительный ответ, вследствие чего воспаление становится хроническим и вялотекущим. Внутриклеточное накопление липидов является необходимым условием инициации атерогенеза, однако неизвестно, является ли оно достаточным. Анализ транскриптома и биоинформатический аппарат позволили охарактеризовать состояние макрофагов, нагруженных липидами. Исследования, представленные в настоящем обзоре, показывают, что реакция врожденного иммунитета способствует накоплению внутриклеточных липидов и усугубляет его.

The accumulation of cholesterol under the influence of modified low density lipoprotein is a key cause of atherogenesis. It is known that atherosclerosis is accompanied by chronic local inflammation. Monocytes/macrophages, main cells of the innate immunity, may not only capturing and accumulating lipids in the vascular wall, but also secreting signaling molecules that affect the functions of other cells. An atherosclerotic lesion is characterized by the inability to complete the inflammatory response, as a result of which the inflammation becomes chronic. Intracellular lipid accumulation is a necessary condition for the initiation of atherogenesis, but it is not known whether it is sufficient. Analysis of the transcriptome allowed us to characterize the state of macrophages loaded with lipids. Studies presented in this review show that the reaction of innate immunity contributes to the accumulation of intracellular lipids and aggravates it.

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