Mолекулярные механизмы сосудистой кальцификации

Сосудистая кальцификация является распространенной и опасной для жизни патологией. Это активный биорегулируемый процесс, который наблюдается в патогенезе целого ряда заболеваний, связанных с нарушением метаболизма, патологиями соединительной ткани и старением. В кальцификации сосудов задействованы сигнальные пути и транскрипционные факторы, которые также играют роль в нормальном остеогенезе и/или в развитии сосудов. В обзоре особое внимание уделено роли сигнальных путей BMP (bone morphogenic protein, костный морфогенный белок), Notch, Wnt [wingless-type MMTV (Mouse Mammary Tumor Virus) integration site family members, член семейства интеграционного сайта ММТВ (мышиный вирус опухоли молочной железы) типа потери крыльев] и роли транскрипционных факторов BMP2, RUNX2, Msx2 в процессе кальцификации. По-видимому, нарушения в функционировании проостеогенных сигнальных путей и приобретение клетками сосудов остеогенного фенотипа характерно не только для минерализации и окостенения сосудов, но и является общим путем деградации сосудов. Проостеогенные изменения на клеточном и молекулярном уровне могут играть роль и в патогенезе заболеваний, в которых минерализация сосудов не проявляется, таких как аневризма грудной аорты. Способность сосудистых клеток приобретать остеофенотип, вероятно, имеет биологический смысл. Чрезмерное ослабление уровня активности остеогенных сигнальных путей также может приводить к патологическим изменениям в сосудах.

Целью представляемого обзора является рассмотрение механизмов сосудистой кальцификации с точки зрения участия сигнальных путей и сосудистых клеток в этом процессе. Главной задачей обзора является исследование причин и механизмов аортальной кальцификации; особый интерес для авторов представляет роль процессов кальцификации в патогенезе аневризмы аорты. Понимание механизмов биологической регуляции про- и антиостеогенных процессов при патологии и в норме открывает возможности воздействовать на этот процесс при коррекции сосудистых патологий.

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