vedomostiregmedРегуляторные исследования и экспертиза лекарственных средствRegulatory Research and Medicine Evaluation3034-30623034-3453Federal State Budgetary Institution ‘Scientific Centre for Expert Evaluation of Medicinal Products’ of the Ministry of Health of the Russian Federation (FSBI ‘SCEEMP’)vedomostiregmed-39Research ArticleОБЗОРНЫЕ И ПРОБЛЕМНЫЕ СТАТЬИGENERAL AND TOPICAL ARTICLESN0 в сигнальном каскаде фармакологического прекондиционирования при ишемии-реперфузии миокардаThe role of NO in signaling pathway in cardiac ischemic preconditioning against myocardial ischemia-reperfusion injuryДаниленкоЛ. М.DanilenkoL. M.Danilenko_L@bsu.edu.ruПокровскийМ. В.PokrovskiyM. V.noemail@neicon.ruДенисюкТ. А.DenysyukT. A.noemail@neicon.ruКолесникИ. М.KolesnikI. M.noemail@neicon.ruАлехинС. А.AlekhinS. A.noemail@neicon.ruБелгородский государственный национальный исследовательский университетРоссияFederal State Autonomous Educational Institution of Higher Professional Education «Belgorod State National Research University»Russian FederationКурский государственный медицинский университетРоссияKursk State Medical UniversityRussian Federation201513022018024044Copyright © Даниленко Л.М., Покровский М.В., Денисюк Т.А., Колесник И.М., Алехин С.А., 20182018Даниленко Л.М., Покровский М.В., Денисюк Т.А., Колесник И.М., Алехин С.А.Danilenko L.M., Pokrovskiy M.V., Denysyuk T.A., Kolesnik I.M., Alekhin S.A.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.vedomostincesmp.ru/jour/article/view/39

Результаты последних исследований подтверждают роль NO в кардиопротекторном эффекте ишемического прекондиционирования (ИП). Влияние оксида азота при ишемической реперфузии, направленное на митохондрию, считается конечной целью кардиопротекции. При прекондиционировании путь начинается в мембране сарколеммы, а затем направляется в цитоплазму посредством множества каскадов энзимов, включая синтазу оксида азота (NOS), растворимую гуанилатциклазу (sGC) и протеинкиназу G (PKG). Таким образом, сигнал передается в митохондрии, где и происходит кардиопротекция. Доказано, что митохондрия осуществляет защиту сердца от ишемически-реперфузионных повреждений с помощью открытия митохондриальных АТФ-зависимых К+-каналов и с помощью преобразования пропускной способности митохондрии. Изучение данных фармакологических подходов может быть использовано при разработке стратегии кардиопротекции в клинике при ишемически-реперфузионных повреждениях миокарда.

Many recent studies have confirmed the effect of NO and that its relative signaling pathway is important for preconditioning of the cardioprotective effect. Mitochondria as a target for the cardioprotective effects of nitric oxide in ischemia-reperfusion injury is considered to be the ultimate goal of cardioprotection. During preconditioning, signaling is initiated from the sarcolemmal membrane and then spread into the cytoplasm via many series of enzymes, including nitric oxide synthase (NOS), soluble guanylyl cyclase (sGC), and protein kinase G (PKG). As a result, the signal is transmitted into the mitochondria, where the cardioprotective effect occurs. It is now well established that mitochondria act to protect the heart against ischemia-reperfusion injury via the opening of the mitochondrial ATP-sensitive K+ channel and the inhibition of mitochondrial permeability transition. This knowledge may be useful in developing novel strategies for clinical cardioprotection from ischemia-reperfusion injury.

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