Статья
Патогенетическая роль тканевого фактора в атеротромбозе и дисфункции эндотелия
Окклюзия просвета сосуда в результате разрыва или эрозии атеросклеротической бляшки, приведшей к тромбозу, лежит в основе таких тяжелых клинических проявлений атеросклероза, как внезапная смерть, инфаркт миокарда и инсульт. В настоящее время установлена ключевая роль тканевого фактора в инициации большинства звеньев коагуляционного каскада, участвующих в возникновении и формировании тромба. Исследования, проведенные в последние годы, позволили расшифровать структуру, пути синтеза тканевого фактора и механизмы его активации. Установлено, что тканевой фактор является основным элементом атеротромбоза и тесно взаимосвязан с иммуновоспалительным процессом, дисфункцией эндотелия, процессами ангиогенеза и клеточной миграции, играющих существенную роль не только в развитии сердечно-сосудистых заболеваний, но и в возникновении воспалительных и онкологических процессов. Имеются данные, свидетельствующие о том, что базальная активность тканевого фактора крови является независимым показателем риска кардиоваскулярных событий, прогнозирует эффективность тромболизиса, а также влияет на результаты ангиопластических операций. Важным представляется проведение оценки возможного влияния на продукцию тканевого фактора таких широко применяемых в клинической практике лекарственных средств, как препараты, используемые для лекарственного покрытия стентов, а также различных групп статинов. Дальнейшее изучение физиологической и патофизиологической роли тканевого фактора позволит расширить имеющиеся представления о патогенезе не только сердечно-сосудистых, но и многих других заболеваний.
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