Молекулярные механизмы взаимодействия ферроптоза и купроптоза при ишемическом инсульте. Фармакологические перспективы предотвращения мозговых нарушений

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Аннотация

Ишемический инсульт является одним из наиболее тяжелых и распространенных неврологических расстройств, представляет значительную угрозу здоровью и продолжительности жизни пострадавших лиц. Ишемический инсульт, возникающий в результате нарушения кровотока, приводит к гипоксии и ишемии мозговой ткани, провоцируя каскад патофизиологических изменений, которые заметно усугубляют повреждение нейронов и могут даже привести к гибели этих клеток. В последние годы новые исследования все больше сосредотачиваются на новых механизмах гибели клеток, таких как ферроптоз и купроптоз. Все больше доказательств подтверждают независимую роль ферроптоза и купроптоза при ишемическом инсульте. Цель обзора — выяснение потенциальных механизмов перекрестной регуляции между ферроптозом и купроптозом, изучение их регуляторной роли при ишемическом инсульте. Подробно исследуеются внутриклеточные взаимодействия ферроптоза и купроптоза при ишемическом инсульте, акцентируя внимание на ключевых аспектах, в частности на фундаментальных функциях железа и меди, метаболические нарушения при ишемическом инсульте, перекрестные влияния и сигнальные пути. Результаты обобщения последних публикаций не только углубляют наше понимание патогенеза ишемического инсульта, но и позволяют предложить новые идеи и направления для будущих фармакологических вмешательств в лечении ишемического инсульта.

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Владимир Иванович Ващенко

Военно-медицинская академия им. С.М. Кирова

Автор, ответственный за переписку.
Email: vladimir-vaschenko@yandex.ru

д-р биол. наук

Россия, Санкт-Петербург

Елена Федоровна Сороколетова

Военно-медицинская академия им. С.М. Кирова

Email: helensoroc@yandex.ru
ORCID iD: 0000-0002-9645-3391

канд. биол. наук

Россия, Санкт-Петербург

Петр Дмитриевич Шабанов

Военно-медицинская академия им. С.М. Кирова

Email: pdshabanov@mail.ru
ORCID iD: 0000-0003-1464-1127
SPIN-код: 8974-7477

д-р мед. наук, профессор

Россия, Санкт-Петербург

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2. Рис. 1. Метаболические пути ферроптоза и их связь с регуляторными путями при ишемическом инсульте. © L. Zhang и соавт., 2024. Адаптировано из [39]. Распространяется на условиях лицензии CC-BY 4.0.

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3. Рис. 2. Упрощенная схема взаимодействия механизмов ферроптоза и купроптоза: ПНЖК — полиненасыщенные жирные кислоты (PUFA); DLAT —дигидроамидацетилтрансфераза; LA — липоевая кислота; GSH — глутатион; FDX1 — ферредоксин 1; LIAS — липоат синтаза; PL-PUFA — фосфатидил полиненасыщенные жирные кислоты; GPX4 — глутатионпеорсидаза 4; p53, p21 — ядерные белки; ATP7A/B — транспортные АТФазы; VDAC — потенциал-зависимые анионные каналы. © Chao M., и соавт. 2024. Адаптировано из [107] с изменениями. Распространяется на условиях лицензии CC-BY 4.0.

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4. Рис. 3. Химические формулы некоторых потенциальных корректоров ферроптора и купроптоза.

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