РОЛЬ микроРНК, NO-СИНТАЗ, КИНАЗ, КАТФ-КАНАЛОВ В ИНФАРКТ-ЛИМИТИРУЮЩЕМ ЭФФЕКТЕ АДАПТАЦИИ К ГИПОКСИИ
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Ключевые слова

сердце
хроническая гипоксия
микроРНК
NO-синтазы
КАТФ-каналы

Как цитировать

Нарыжная, Н. В., Воронков, Н. С., Скрябина, А. А., Бушов, Ю. В., & Маслов, Л. Н. (2019). РОЛЬ микроРНК, NO-СИНТАЗ, КИНАЗ, КАТФ-КАНАЛОВ В ИНФАРКТ-ЛИМИТИРУЮЩЕМ ЭФФЕКТЕ АДАПТАЦИИ К ГИПОКСИИ. Российский физиологический журнал им. И. М. Сеченова, 106(1), 3–16. https://doi.org/10.31857/S0869813920010112

Аннотация

Установлено, что хроническая гипоксия (ХГ) существенно изменяет экспрессию микроРНК в миокарде. Показано, что miR-138 и miR-184 усиливают толерантность кардиомиоцитов к гипоксии, а microRNA‑199a‑5p и miR-23b снижают устойчивость этих клеток к гипоксии. ХГ усиливала экспрессию индуцибельной (iNOS) и эндотелиальной NO-синтазы (eNOS). Показано, что кардиопротекторный эффект ХГ связан с активацией iNOS. Установлено, что изоформы δ и ε протеинкиназы С участвуют в кардиопротекторном эффекте адаптации к гипоксии. Показано, что ХГ вызывает усиление экспрессии киназ CaMKII, p-ERK1/2, p-p38, p-Akt, гексокиназы-1, гексокиназы-2. Гипоксия усиливает транслокацию гексокиназы-2 в митохондрии. У животных, адаптированных к гипоксии, не удалось обнаружить увеличения экспрессии киназ: ПКA, p-GSK3β, AMPK и JNK. Представлены данные, указывающие на то, что киназы ERK1/2, MEK1/2 участвуют в кардиопротекторном эффекте адаптации к гипоксии. Гипертрофия миокарда, вызванная хронической гипоксией, связана с активацией Rho-киназы. Вопрос о роли PI3, Akt JNK, PKG, Rho-киназы, mTOR и p38 в защитном эффекте адаптации к гипоксии является спорным. Установлено, что инфаркт-лимитирующий эффект ХГ зависит от активации митоКАТФ-каналов. Цель обзора: анализ данных о роли микроРНК, NO-синтазы и киназ в кардиопротекторном эффекте ХГ.

https://doi.org/10.31857/S0869813920010112
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