МЕТАБОЛИЧЕСКОЕ РЕПРОГРАММИРОВАНИЕ МИКРОГЛИИ И АСТРОЦИТОВ, КАК ФАКТОР РЕГУЛЯЦИИ НЕЙРОВОСПАЛЕНИЯ ПРИ ИШЕМИЧЕСКОМ ИНСУЛЬТЕ
https://doi.org/10.15789/1563-0625-MRO-3131
Аннотация
Резюме
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.
Ключевые слова
Об авторах
Михаил Юрьевич БобровРоссия
кандидат химических наук, ведущий научный сотрудник, направление "Иммунобиология и биомедицина", центр генетики и наук о жизни
Вадим Сергеевич Никитин
Россия
лаборант-исследователь, студент магистратуры НТУ «Сириус», Направления «Иммунобиология и биомедицина»
Марина Юрьевна Бурак
Россия
лаборант-исследователь, студент магистратуры НТУ «Сириус», Направления «Иммунобиология и биомедицина»
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Бобров М.Ю., Никитин В.С., Бурак М.Ю. МЕТАБОЛИЧЕСКОЕ РЕПРОГРАММИРОВАНИЕ МИКРОГЛИИ И АСТРОЦИТОВ, КАК ФАКТОР РЕГУЛЯЦИИ НЕЙРОВОСПАЛЕНИЯ ПРИ ИШЕМИЧЕСКОМ ИНСУЛЬТЕ. Медицинская иммунология. https://doi.org/10.15789/1563-0625-MRO-3131
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Bobrov M., Nikitin V., Burak M. METABOLIC REPROGRAMMING OF MICROGLIA AND ASTROCYTES AS A FACTOR IN THE REGULATION OF NEUROINFLAMMATION IN ISCHEMIC STROKE. Medical Immunology (Russia). (In Russ.) https://doi.org/10.15789/1563-0625-MRO-3131