Модифицирование тайтина как потенциальный метод лечения хронической сердечной недостаточности с сохраненной фракцией выброса

Хроническая сердечная недостаточность с сохраненной фракцией выброса (ХСНсФВ) является многофакторным состоянием с различными патофизиологическими причинами и морфологическими проявлениями, что во многом обуславливает применение терапевтических подходов, адаптированных к клиническому фенотипу пациента. В последние годы ХСНсФВ все более активно замещает хроническую сердечную недостаточность со сниженной фракцией выброса (ХСНнФВ) и представляет собой не менее тяжелое состояние, снижающее качество жизни пациентов наравне с ХСНнФВ. В настоящее время ХСНсФВ страдает около 9 % людей старше 60 лет, а выживаемость в течение 5 лет при этой форме ХСН составляет около 35 %. Современный набор лекарственных препаратов для коррекции проявлений ХСНсФВ достаточно ограничен. Одним из возможных решений является воздействие на процессы модификации и, как следствие, механические свойства тайтина — одного из основных белков саркомера мышечной ткани. На данный момент ведутся активные исследования по разработке и использованию препаратов, влияющих на модифицирование тайтина, а также их доклинические и клинические испытания. В обзоре рассматриваются структура и процессы модификации (преимущественно — фосфорилирования) тайтина, различные сигнальные пути, патологии которых ассоциированы с развитием ХСНсФВ, а также данные исследований по применению препаратов, воздействующих на эти сигнальные пути, у животных и людей. Приводятся результаты анализа отечественной и зарубежной литературы, опубликованной в период с 2000 по 2026 гг. на платформах PubMed, Elsevier, Google Scholar и др. Текущие данные свидетельствуют о том, что воздействие на модифицирование тайтина является потенциально эффективным методом для лечения хронической сердечной недостаточности, что указывает на необходимость дальнейших исследований в данной области для поиска новых фармакологических решений и введения их в клиническую практику с целью персонализированного лечения синдрома ХСНсФВ.

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