mimmunМедицинская иммунологияMedical Immunology (Russia)1563-06252313-741XSPb RAACI10.15789/1563-0625-MRO-3131mimmun-3131Research ArticleОБЗОРЫREVIEWSМетаболическое репрограммирование микроглии и астроцитов как фактор регуляции нейровоспаления при ишемическом инсультеMetabolic reprogramming of microglia and astrocytes is a regulatory factor of neuroinflammation in ischemic strokehttps://orcid.org/0000-0002-5837-473XБобровМ. Ю.BobrovM. Yu.

кандидат химических наук, ведущий научный сотрудник, направление "Иммунобиология и биомедицина", Научный центр генетики и наук о жизни

PhD (Chemistry), Leading Researcher, Department of Immunobiology and Biomedicine, Scientific Center of Genetics and Life Science

bobrov.my@talantiuspeh.ruНикитинВ. С.NikitinV. S.

лаборант-исследователь, студент магистратуры, направление «Иммунобиология и биомедицина», Научный центр генетики и наук о жизни

Laboratory Researcher, Master Student, Sirius University, Department of Immunobiology and Biomedicine, Scientific Center of Genetics and Life Science

vadim-nikitin2100@mail.ruБуракМ. Ю.BurakM. Yu.

лаборант-исследователь, студент магистратуры, направление «Иммунобиология и биомедицина», Научный центр генетики и наук о жизни

Laboratory Researcher, Master Student, Department of Immunobiology and Biomedicine, Scientific Center of Genetics and Life Science

burak.my@talantiuspeh.ruАНОО ВО «Научно-технологический университет «Сириус», федеральная территория «Сириус»РоссияSirius University of Science and Technology (Sirius University)Russian Federation20252012202527611611180Copyright © Бобров М.Ю., Никитин В.С., Бурак М.Ю., 20252025Бобров М.Ю., Никитин В.С., Бурак М.Ю.Bobrov M.Y., Nikitin V.S., Burak M.Y.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.mimmun.ru/mimmun/article/view/3131

Ишемический инсульт является одним из самых распространенных заболеваний во всем мире, с высоким уровнем заболеваемости и смертности. В патологическом процессе ишемии нервной ткани нейровоспаление является важным фактором, который определяет функциональный прогноз исхода заболевания. При формировании ишемического очага происходит активация клеток микроглии, а также астроцитов, что приводит к запуску каскада нейровоспалительных реакций, играющих важную роль в патофизиологии ишемического инсульта. Активированные клетки микроглии и астроциты способны формировать разнообразные фенотипы в зависимости от соответствующих параметров микроокружения. Данные фенотипы могут оказывать как нейротоксическое, так и нейропротекторное действие. С одной стороны, при повреждении нервной ткани глиальные клетки способствуют удалению клеточного дебриса, поддержанию ионного гомеостаза, регулируют внеклеточное содержание нейротрансмиттеров и обеспечивают трофику нейронов. С другой стороны, микроглия и астроциты могут приобретать провоспалительный фенотип, характеризующийся секрецией воспалительных цитокинов, который способствует прогрессированию нейровоспаления и повреждению тканей. Таким образом, астроциты и микроглия претерпевают как морфологические, так и функциональные перестройки, тем самым активно участвуя в нейровоспалении за счет высвобождения провоспалительных или противовоспалительных факторов. Важно отметить, что эти перестройки сопряжены с метаболическим репрограммированием, которое приводит к изменению активности метаболических путей для компенсации дефицита энергии и строительных материалов, вызванного нарушением мозгового кровотока. Провоспалительный фенотип микроглии характеризуется активацией гликолиза, пентозофосфатного пути, синтеза жирных кислот и глутамина, тогда как противовоспалительный фенотип демонстрирует усиление окислительного фосфорилирования и окисления жирных кислот. Для реактивных астроцитов характерно усиление гликолиза, гликогенолиза и сниженное поглощение глутамата. В последнее время появляется все больше свидетельств того, что манипулирование гомеостазом глиальных клеток может быть использовано для переключения с нейротоксического фенотипа на нейропротекторный. Всестороннее понимание основных механизмов переключения метаболических фенотипов потенциально может позволить направленно репрограммировать глиальные клетки в ходе патологического процесса, что может быть использовано в терапевтических подходах для лечения последствий ишемического инсульта. В данном обзоре представлены современные представления о метаболическом репрограммировании в астроцитах и клетках микроглии в контексте патофизиологических процессов при ишемии мозга.

Ischemic stroke is one of the most common diseases worldwide, with a high incidence and mortality rate. In the pathological process of ischemia of nervous tissue, neuroinflammation is an important factor that determines the functional prognosis of the outcome of the disease. During the formation of an ischemic focus, microglial cells and astrocytes are activated, which leads to the launch of a cascade of neuroinflammatory reactions that play an important role in the pathophysiology of ischemic stroke. Activated microglial cells and astrocytes are able to form a variety of phenotypes depending on the corresponding parameters of the microenvironment. These phenotypes can have both neurotoxic and neuroprotective effects. On the one hand, when nerve tissue is damaged, glial cells contribute to the removal of cellular debris, maintain ionic homeostasis, regulate the extracellular content of neurotransmitters and ensure the trophism of neurons. On the other hand, microglia and astrocytes can acquire a pro-inflammatory phenotype characterized by the secretion of inflammatory cytokines, which contributes to the progression of neuroinflammation and tissue damage. Thus, astrocytes and microglia undergo both morphological and functional rearrangements, thereby actively participating in neuroinflammation due to the release of pro-inflammatory or anti-inflammatory factors. It is important to note that these rearrangements are associated with metabolic reprogramming, which leads to a change in the activity of metabolic pathways to compensate for the lack of energy and building materials caused by impaired cerebral blood flow. The pro-inflammatory phenotype of microglia is characterized by activation of glycolysis, the pentose phosphate pathway, synthesis of fatty acids and glutamine, whereas the anti-inflammatory phenotype demonstrates increased oxidative phosphorylation and oxidation of fatty acids. Reactive astrocytes are characterized by increased glycolysis, glycogenolysis and reduced glutamate uptake. Recently, there has been increasing evidence that manipulation of glial cell homeostasis can be used to switch from a neurotoxic phenotype to a neuroprotective one. A comprehensive understanding of the basic mechanisms of switching metabolic phenotypes can potentially allow targeted reprogramming of glial cells during the pathological process, which can be used in therapeutic approaches for the treatment of the consequences of ischemic stroke. This review presents current ideas about metabolic reprogramming in astrocytes and microglial cells in the context of pathophysiological processes in cerebral ischemia.

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