[Mitochondrial Dysfunction in Mechanisms of Atherogenesis] (original) (raw)
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Mitochondria import hundreds of different precursor proteins from the cytosol, and only 13 proteins are encoded by mtDNA itself. Recent investigations demonstrated real size of mitochondrial proteome and complexity of their functions There are many methods using for mitochondrial proteome profiling, that help to understand a molecular mechanisms of mitochondrial functions and identify the causes of disruptions that lead to different disorders. In this review we discuss a recent data in the field of mitochondrial proteomics.
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Изучены возможности лазерной конфокальной микроскопии в анализе объема липидных частиц и количества функционально-активных митохондрий и продукции активных форм кислорода в клетках печени для ранней диагностики цитохимических нарушений при дислипопротеидемии. Оценен потенциал анализа уровня мтДНК плазмы крови на ранних сроках развития дислипопротеидемии и при экспериментальном инфаркте миокарда. Полученные данные будут служить основой для создания технологий диагностического мониторинга выраженности атеросклероза и инфаркта миокарда.
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The article concerns the contribution of mitochondrial dysfunction to the development of inflammatory joint diseases. Mitochondria are the main suppliers of adenosine triphosphate (ATP). Reactive oxygen species (ROS) are a by-product of this metabolic process. Mitochondria also have an effective antioxidant mechanism: there is a certain balance between the ROS formation and their inactivation. Accumulation with age of mutations (single nucleotide substitutions, e.g., transversions, transitions, and deletions) in mitochondrial DNA, may cause a disorder in selective destruction (utilization) of damaged and dysfunctional mitochondria (mitophagy) thus leading to imbalance between the ROS production and their neutralization. This process is triggered by both internal factors (ROS overproduction) and external factors, i.e., tissue damage / injury and infection. The failure of quality control mechanisms resulting from disruption of mitophagy leads to a significant increase in terminally da...
Protein markers of mitochondria formation and alteration in patients with impaired blood circulation
The Scientific Notes of the I. P. Pavlov St. Petersburg State Medical University
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1 Балтийский федеральный университет им. Иммануила Канта, 236038 Калининград, Россия; электронная почта: IMazunin@kantiana.ru 2 Сибирский институт физиологии и биохимии растений Сибирского отделения Российской академии наук, 664033 Иркутск, Россия; электронная почта: yukon@sifibr.irk.ru 3 Иркутский государственный университет, 664003 Иркутск, Россия 4 Московский государственный университет им. М.В. Ломоносова, 119991 Москва, Россия; электронная почта: peter@protein.bio.msu.ru Поступила в редакцию 03.12.17 После доработки 12.02.18