Механизмы структурного ремоделирования миокарда на фоне воздействия вибрации
- Авторы: Воробьева В.В.1,2, Левченкова О.С.3, Ленская К.В.2, Шабанов П.Д.1
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Учреждения:
- Военно-медицинская академия им. С.М. Кирова
- Санкт-Петербургский государственный университет
- Смоленский государственный медицинский университет
- Выпуск: Том 22, № 1 (2024)
- Страницы: 17-32
- Раздел: Научные обзоры
- URL: https://journals.rcsi.science/RCF/article/view/258597
- DOI: https://doi.org/10.17816/RCF624185
- ID: 258597
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Аннотация
В обзоре представлен анализ литературных источников, посвященных изучению структурных изменений со стороны сердца у пациентов с вибрационной болезнью, выявленных с помощью эхокардиографических методов исследования в виде концентрического ремоделирования камер левого желудочка и нарушения его диастолической функции, снижения интенсивности работы структур сердца по сравнению со здоровыми людьми в 1,2 раза (р < 0,05). Анализ морфометрических и биоэнергетических показателей кардиомиоцитов на фоне различных экспериментальных режимов вибрации (7 и 56 сеансов с частотой 8 Гц) подтверждает нарушение идеального соотношения между пространственной конфигурацией полостей сердца, способностью к сокращению и обеспеченностью энергетическим потенциалом. Утрата миофибрилл клетками сердца символизирует переход гипертрофии миокарда в стадию декомпенсации и нарастание дегенеративных (дистрофических) признаков, в частности утраты саркомеров кардиомиоцитов. Для реализации процессов патологической структурной (морфологической) и энергетической перестройки ткани под воздействием вибрационно-опосредованных гемодинамических и ишемических факторов необходимо вовлечение в процесс многочисленных посредников, регулирующих метаболизм, пролиферацию, рост и выживание клеток, таких как STIM (молекула стромального взаимодействия), SERCA (кальциевая аденозинтрифосфатаза эндо(сарко)плазматического ретикулума), IP3R (рецептор инозитол-1,4,5-трифосфата), Orai (белок, формирующий CRAC каналы), TRPС (канонические каналы транзиторного рецепторного потенциала) и др. В качестве одного из важнейших звеньев структурного ремоделирования сердца выступает система деградации экстрацеллюлярного матрикса, включающая матриксные металлопротеиназы и их тканевые ингибиторы, регулирующие скорость синтеза мРНК на матрице ДНК путем связывания со специфическими участками ДНК контроля сердечной трофики и пластичности. Большое количество проанализированных фактов позволяет объяснить некоторые закономерности развития ремоделирования сердца у пациентов с вибрационной болезнью и определить направленность патогенетически обоснованных подходов к терапии с учетом не только вибропротективного эффекта лекарственных препаратов, но и их способности торможения и регресса ремоделирования миокарда.
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Виктория Владимировна Воробьева
Военно-медицинская академия им. С.М. Кирова; Санкт-Петербургский государственный университет
Email: v.v.vorobeva@mail.ru
ORCID iD: 0000-0001-6257-7129
SPIN-код: 2556-2770
д-р мед. наук
Россия, Санкт-Петербург; Санкт-ПетербургОльга Сергеевна Левченкова
Смоленский государственный медицинский университет
Email: levchenkova-o@yandex.ru
ORCID iD: 0000-0002-9595-6982
SPIN-код: 2888-6150
д-р. мед. наук
Россия, СмоленскКарина Владимировна Ленская
Санкт-Петербургский государственный университет
Email: karinavl@mail.ru
ORCID iD: 0000-0002-6407-0927
д-р биол. наук, профессор
Россия, Санкт-ПетербургПетр Дмитриевич Шабанов
Военно-медицинская академия им. С.М. Кирова
Автор, ответственный за переписку.
Email: pdshabanov@mail.ru
ORCID iD: 0000-0003-1464-1127
SPIN-код: 8974-7477
д-р мед. наук, профессор
Россия, Санкт-ПетербургСписок литературы
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