Exosomes and exomeres are the smallest microparticles ranging from 20 to 130 nm in diameter. They are found in almost all biological fluids. Exosomes and exomeres are of considerable interest since they can be involved in intercellular signaling and are biological markers of the state of cells, which can be used for diagnostics. The nomenclature of exosomes remains poorly developed. Most researchers try to classify them based on the mode of formation, physicochemical characteristics, and the presence of tetrasporin markers CD9, CD63, and CD81. The data presented in this work show that although exomeres carry tetrasporin biomarkers, they differ from exosomes strongly in lipid composition, especially in cholesterol content. The production of exomeres by cells is associated with the synthesis of cholesterol in cells and is expressed or suppressed by regulators of the synthesis of mevalonate, an intermediate product of cholesterol metabolism. In addition, the work shows that the concentration of extracellular particles in the body correlates with the concentration of cholesterol in the plasma, but weakly correlates with the concentration of cholesterol in lipoproteins. This suggests that not all plasma cholesterol is associated with lipoproteins, as previously thought.

According to the World Health Organization, about 5 million people die every year from cerebrovascular disease. At the same time, the proportion of cerebral infarction, or ischemic stroke (IS), among forms of acute cerebrovascular accident reaches 80-85%. Despite the active study of biochemical and morphological changes leading to acute cerebrovascular ischemia, the problem of early diagnosis, prevention, as well as predicting the outcome of this disease is still relevant. There is no doubt that the interruption of the ischemic cascade at earlier stages can be accompanied by a greater effect of treatment. A timely and effective pharmacological intervention requires a clear understanding of the pathochemical and biological processes underlying acute ischemia at the molecular level. High mortality and disability accompanying acute IS, dictate the need to create new diagnostic and prognosis algorithms both in the acute period of IS, and in the recovery period. According to some authors, elucidation of the pathways that underlie the pathogenetic mechanisms acting in the penumbra are of great clinical interest for the development of new diagnostic and therapeutic strategies. Studying the mechanisms of apoptosis and autophagy of neurons in the dynamics of the acute period of IS, modulation of the autophagy process in the penumbra zone can contribute to the development of new methods for the diagnosis and treatment of acute IS. The review presents the results of the latest experimental studies on the role of apoptosis and autophagy in the development of acute cerebral ischemia and attempts to modulate these processes in order to influence the ischemic cascade. The review was based on sources from such international and national data bases as Scopus, Web of Science, Springer, RINC.

В течение последних десятилетий острый ишемический инсульт (ОИИ) является актуальной медицинской и социальной проблемой. Высокая смертность и инвалидизация, сопровождающие ОИИ, диктуют необходимость создания новых алгоритмов профилактики, диагностики и прогноза исхода заболевания. Помочь в этом могут надежные биологические маркеры и высокотехнологичные методы лабораторной диагностики. Результаты новейших исследований свидетельствуют о том, что апоптоз, аутофагия и некроз являются основными механизмами гибели нейронов при ОИИ. Тем не менее до конца не ясно, какой из этих процессов преобладает на конкретном этапе ишемического каскада и в большей степени влияет на исход заболевания. Исследования в области нейроиммунологии позволили установить сигнальные белки, инициирующие как апоптотическую, так и аутофагическую гибель клеток головного мозга при ОИИ. Эти белки действуют либо синергично за счет создания общих модулей, либо альтернативно, в качестве переключателей с одной клеточной программы на другую. По мнению ученых, исследование перекрестных взаимодействий между апоптозом и аутофагией и их отдельными медиаторами в патогенезе ОИИ представляет большой интерес. Сравнительная оценка динамики концентрации биомаркеров аутофагии и апоптоза в периферической крови пациентов с ОИИ в сопоставлении с динамикой тяжести неврологического дефицита и объемом поражения головного мозга поможет глубже понять перекрестные взаимодействия между этими процессами на разных этапах острого периода ишемического инсульта. По мнению ряда авторов, исследование белков, участвующих в индукции аутофагии и апоптоза при ОИИ, будет способствовать не только более глубокому пониманию патогенеза заболевания, но и созданию новых диагностических алгоритмов, разработке специфических биомаркеров, предикторов течения и исхода заболевания. Ключевые слова: апоптоз, аутофагия, острый ишемический инсульт, биомаркеры аутофагии, биомаркеры апоптоза, вестерн-блоттинг, проточная цитометрия.

Apoptosis, along with proliferation, is a form of lymphocyte response to activating stimuli. In the early stages of cell differentiation, the apoptotic response prevails and it results to the formation of tolerance to inductor antigen. Mature lymphocytes proliferate in response to stimulation and it means the initial stage in the development of the immune response. Since in this case apoptosis and proliferation acts as alternative processes, their ratio can serve as a measure of the effectiveness of the cellular response to activating signals. The resistance of autoreactive T-cells to apoptosis is the main key point in the development of type 1 diabetes mellitus (T1DM). Autoreactive T-cells migrates from the bloodstream to the islet tissue of the pancreas and take an active part in b cells destruction. The resistance of autoreactive effector T-cells to apoptosis may suggest their high proliferative potential. Therefore, the comparative evaluation of apoptosis and proliferation of peripheral blood lymphocytes can give a more complete picture of their functional state and thus will help to reveal the causes of ineffective peripheral blood T-ceiis apoptosis in patients with T1DM and will help to understand more deeply the pathogenesis of the disease. in this article, the features of proliferative response of peripheral blood T-cells in patients with T1DM and in individuals with high risk of developing T1DM have been studied. Apoptosis of T-cell subpopulations has been investigated. The correlation between the apoptotic markers and the intensity of spontaneous and activation- induced in vitro T-cells proliferation of was revealed. it was determined, that autoreactive peripheral blood T-cells were resistant to apoptosis and demonstrated the increased proliferative potential in patients with T1DM and in individuals with high risk of developing T1DM.

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