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Молекулярная биология, 2023, T. 57, № 3, стр. 427-439

Как гистондеацетилаза 3 контролирует экспрессию гепсидина и репликацию вируса гепатита С

А. С. Щербакова a, С. Н. Кочетков a, М. В. Козлов a, *

a Институт молекулярной биологии им. В.А. Энгельгардта Российской академии наук
119991 Москва, Россия

* E-mail: kozlovmavi@gmail.com

Поступила в редакцию 28.09.2022
После доработки 25.11.2022
Принята к публикации 25.11.2022

Аннотация

Ключевую роль гистондеацетилаз (HDAC) в регуляции клеточного ответа на заражение вирусом гепатита С (HCV) впервые продемонстрировали в 2008 году. Изучая метаболизм железа в тканях печени больных хроническим гепатитом С, обнаружили, что в условиях окислительного стресса, вызванного вирусной инфекцией, в гепатоцитах заметно снижается экспрессия гена гепсидина (HAMP), гормона-регулятора экспорта железа. В схему регуляции экспрессии гепсидина оказались вовлечены HDAC, контролирующие уровень ацетилирования гистонов и транскрипционных факторов, прежде всего STAT3, ассоциированных с промотором HAMP. В настоящем обзоре обобщены современные данные о функционировании регуляторного контура HCV-HDAC3-STAT3-HAMP как пример хорошо охарактеризованного взаимодействия вируса и эпигенетического аппарата клетки-хозяина.

Ключевые слова: вирус гепатита С, репликация, STAT3, гепсидин, окислительный стресс, гистондеацетилаза 3, регуляция экспрессии

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