Роль биомолекул в развитии и прогрессировании кальцификации сосудов при сердечно-сосудистых заболеваниях

Сердечно-сосудистые заболевания (ССЗ) остаются наиболее актуальной проблемой в системе здравоохранения. В патогенез ССЗ вовлечены сложные взаимодействия между изменениями интима-медиа артерий и компонентами крови (накопление липидов, сложных углеводов, фиброзной ткани, кальцификация и др.). В развитии и прогрессировании кальцификации коронарных артерий огромную роль играют различные биомолекулы, где в качестве ингибиторов кальцификации чаще всего выступают остеопонтин, остеопротегерин, склеростин, фетуин-А, неорганический пирофосфат, матриксный Gla-протеин, фактор роста фибробластов 23 (FGF-23), Клото, белки морфогенеза костей (BMP), в частности BMP-7; а активаторов – лептин, BMP-2, BMP-4, паратиреоидный гормон, кальцитриол и др. В настоящее время наиболее изученными биомолекулами, ассоциированными с кальциевым обменом, считаются остеопротегерин, остеопонтин, остеонектин, остеокальцин и белок Клото.

В работе описаны малоизученные эффекты ингибиторов кальцификации (склеростин, фетуин А, матриксный Gla-протеин, FGF-23, неорганический пирофосфат, BMP-7), а также некоторых активаторов кальцификации (лептин, BMP-2 и BMP-4, паратиреоидный гормон и кальцитриол).

Цель данного исследования заключается в анализе и систематизации данных о роли биомолекул в развитии и прогрессировании кальцификации сосудов при ССЗ.

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