The Mitochondrial Permeability Transition Pore – a Regulator of the Resistance of the Heart to Reperfusion / N. V. Naryzhnaya, L. N. Maslov, Yu. B. Lishmanov [et al.]

Уровень набора: Neuroscience and Behavioral Physiology = 1967-Альтернативный автор-лицо: Naryzhnaya, N. V., Nataliya Vladimirovna;Maslov, L. N., Leonid Nikolaevich;Lishmanov, Yu. B., specialist in the field of medical technology, lead engineer aof Tomsk Polytechnic University, doctor of medical sciences, 1951-, Yury Borisovich;Nesterov, E. A., Physicist, Specialist in the field of nuclear power engineering, Researcher of Tomsk Polytechnic University, 1976-, Evgeny Alexandrovich;Jaggi, A. S., Amteshwar Singh;Suleiman, S., SaadehКоллективный автор (вторичный): Национальный исследовательский Томский политехнический университет (ТПУ), Физико-технический институт (ФТИ), Лаборатория № 31 ядерного реактора (Лаборатория № 31 ЯР)Язык: английский ; резюме, eng.Страна: .Резюме или реферат: The most important event in the formation of reperfusion injury to the heart has been shown to be the opening of mitochondrial permeability transition pores (mPTP). mPTP opening is followed by activation of apoptosis, necroptosis, and cardiomyocyte death. Experimental studies have shown that inhibition of mPTP opening decreases infarct size and that conditioning actions on the myocardium are mediated via decreases in the sensitivity of mPTP to opening factors. The present article reviews existing data on the structure and regulation of mPTP in conditions of reperfusion injury to the heart..Примечания о наличии в документе библиографии/указателя: [References: 130 tit.].Аудитория: .Тематика: электронный ресурс | труды учёных ТПУ | myocardium | reperfusion | MPT pores | mitochondria | миокард | реперфузия | митохондрии Ресурсы он-лайн:Щелкните здесь для доступа в онлайн
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[References: 130 tit.]

The most important event in the formation of reperfusion injury to the heart has been shown to be the opening of mitochondrial permeability transition pores (mPTP). mPTP opening is followed by activation of apoptosis, necroptosis, and cardiomyocyte death. Experimental studies have shown that inhibition of mPTP opening decreases infarct size and that conditioning actions on the myocardium are mediated via decreases in the sensitivity of mPTP to opening factors. The present article reviews existing data on the structure and regulation of mPTP in conditions of reperfusion injury to the heart.

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