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Успехи современной биологии, 2023, T. 143, № 4, стр. 335-358

Активация тромбоцитов и механизмы формирования тромбоэмболий у больных с тяжелым течением COVID-19. Альтернативные механизмы деятельности системы гемостаза

Б. И. Кузник 1, Ю. Н. Смоляков 1, *, Н. Н. Цыбиков 1, К. Г. Шаповалов 1

1 Читинская государственная медицинская академия
Чита, Россия

* E-mail: smolyakov@rambler.ru

Поступила в редакцию 27.03.2023
После доработки 04.05.2023
Принята к публикации 05.05.2023

Аннотация

В обзоре освещается механизм развития гиперкоагуляции и тромбообразования при тяжелых формах течения COVID-19. Внедрение в организм хозяина SARS-CoV-2 осуществляется при взаимодействии шиповидного белка S с ангиотензинпревращающим ферментом АСЕ2, находящимся в альвеолоцитах 2-го типа, эндотелии сосудов, почках, печени и других органах. B случае развития тяжелого состояния у больных COVID-19 активируется как неспецифический, так и адаптивный иммунитет. Стимуляция системы комплемента с появлением фрагментов С3а, C3b, C5a и мембраноатакующего комплекса создает условия для развития гиперкоагуляции. Вовлечение в этот процесс ренин-ангиотензин-альдостероновой системы и появление ангиотензина 2 (Ang II) еще сильнее увеличивает интенсивность гиперкоагуляции. При внедрении SARS-CoV-2 в клетки защитная реакция адаптивной иммунной системы может превращаться в патологическую – развивается цитокиновый шторм, характеризующийся высоким уровнем провоспалительных цитокинов (IL-1α, IL-6, IL-8, TNF-α, IL-17 и др.) и хемокинов (ССL2, CCL11 и др.), что в конечном итоге ведет у тяжелобольных COVID-19 к развитию тромбоангиопатии или, иначе, иммунотромбозу. У пациентов с более тяжелым поражением может развиться состояние, подобное синдрому диссеминированного внутрисосудистого свертывания (ДВС). При этом у пациентов с COVID-19 выявляется легкая тромбоцитопения, повышенный уровень фибриногена, D-димера, продуктов деградации фибриногена, что свидетельствует об интенсивном тромбообразовании, а также сокращенные показатели протромбинового времени (ПВ) и активированного частичного тромбопластинового времени (АЧТВ), обусловленные в значительной степени увеличенным уровнем FVIII. При COVID-19, наряду с классическим, проявляется альтернативный путь (минуя тромбин) регуляции системы гемостаза и тромбообразования, связанный в основном с влиянием шиповидного белка S SARS-CoV-2 и папаиноподобной протеазы. Шиповидный белок S непосредственно влияет на переход фибриногена в фибрин и протромбина в тромбин, а также на активацию отдельных плазменных факторов свертывания крови. Альтернативный путь свертывания крови также обусловлен активацией системы комплемента по лектиновому пути с включением металлопротеиназ MASP-1, -2, -3. Кроме того, шиповидный белок S активирует tPA, что может сопровождаться гиперфибринолизом. У тяжелобольных COVID-19 далеко не последняя роль в возникновении тромбоэмболических осложнений принадлежит тромбоцитам. В процессе реакции высвобождения тромбоциты выбрасывают из цитоплазмы в кровь α- и плотные гранулы, содержащие воспалительные цитокины и хемокины, что усиливает цитокиновый шторм и, следовательно, тромбообразование. Воздействуя на шиповидный белок S, тромбоциты запускают альтернативный механизм системы гемостаза и тромбообразования.

Ключевые слова: COVID-19, тромбоциты, шиповидный белок S, система комплемента, цитокиновый шторм, нейтрофилы, моноциты, гиперкоагуляция, тромбообразование, альтернативные механизмы

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