Mедиаторы и сигнальные пути развития миокардиального фиброза

Миокардиальный фиброз тесно связан с тяжелыми сердечно-сосудистыми заболеваниями (ССЗ), характеризующимися повышенными показателями смертности в мире. В основе развития миокардиального фиброза лежит дифференцировка фибробластов в миофибробласты, в избытке синтезирующие компоненты внеклеточного матрикса. Ключевым регулятором дифференцировки фибробластов в миофибробласты является трансформирующий фактор роста бета. В последние годы пристальное внимание в патогенезе фиброза отводится и другим факторам роста, в частности нейротрофинам. Недавно обнаружено, что фибробласты экспрессируют нейротрофический фактор головного мозга (brain-derived neurotrophic factor, BDNF), а его рецепторы вовлечены в патогенез развития фиброза различных органов и тканей. Роль BDNF и его рецепторов в патогенезе миокардиального фиброза только начинает изучаться. Представленный обзор обобщает информацию, имеющуюся в научной литературе (с 2019 по 2023 гг.), посвященную патофизиологическим и патогенетическим механизмам взаимосвязи BDNF с фиброзом сердца. Согласно проанализированным данным, механизмы действия BDNF в сердечно-сосудистой системе и патогенез фиброза сердца имеют общие точки пересечения, что делает нейротрофин многообещающей терапевтической целью при фиброзе сердца. Дальнейшее исследование этих аспектов позволит использовать разносторонние эффекты BDNF для разработки технологий профилактики фиброза сердца.

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