δ-Опиоидный рецептор – мишень для создания пептидных препаратов, повышающих резистентность сердца к реперфузии

δ-Опиоидный рецептор – мишень для создания пептидных препаратов, повышающих резистентность сердца к реперфузии

Автор: Мухомедзянов А.В., Попов С.В., Нарыжная Н.В., Сиротина М.А., Маслов Л.Н., Курбатов Б.К., Горбунов А.С., Килин М., Кан А., Крылатов А.В., Подоксёнов Ю.К., Азев В.Н., Ласукова Т.В., Суфианова Г.З., Хлёсткина М.С.

Журнал: Сибирский журнал клинической и экспериментальной медицины @cardiotomsk

Рубрика: Обзоры и лекции

Статья в выпуске: 1 т.39, 2024 года.

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Анализ опубликованных данных и результатов собственных исследований показал, что активация периферических δ2-опиоидных рецепторов (δ2-ОР) повышает толерантность сердца к реперфузии. Установлено, что δ2-ОР находятся в кардиомиоцитах. Эндогенные опиоиды не участвуют в регуляции устойчивости сердца к реперфузии у неадаптированных крыс. Инфаркт-лимитирующий эффект агониста δ2-ОР дельторфина II зависит от активации протеинкиназ – ПКСδ, ERK1/2, PI3K, ПКG. Гипотетическими конечными эффекторами кардиопротекторного действия дельторфина II являются саркКАТФ-каналы и MPT-поры.

Сердце, реперфузия, инфаркт миокарда, опиоидные рецепторы, киназы, КАТФ-каналы, MPT-пора

Короткий адрес: https://sciup.org/149144770

IDR: 149144770   |   DOI: 10.29001/2073-8552-2022-585

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