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Том 15 №3 2013 год - Нефрология и диализ

Система самозащиты почки: современный взгляд на механизмы,определяющие течение и исход гломерулонефрита (Обзор литературы)


Бобкова И.Н. Чеботарева Н.В. Козловская Л.В. Непринцева Н.В.

Аннотация: В настоящее время среди механизмов, определяющих течение и исход заболеваний почек, наиболее изучены повреждающие (эффекторные) звенья патогенеза – формирование клеточного воспалительного инфильтрата, высвобождение воспалительных цитокинов, метаболитов арахидоновой кислоты и кислородных радикалов, активация компонентов комплемента. Однако степень поражения ткани почки зависит от баланса локально воздействующих повреждающих факторов и противостоящих им эндогенных медиаторов, ограничивающих развитие патологического процесса, что представляет особый интерес для понимания основных закономерностей прогрессирования поражения почек. В обзоре изложены современные представления о «самозащите» почки как об универсальном механизме многоуровневого регулируемого синтеза защитных медиаторов – внутри- и внеклеточного, а также на поверхности клеток. Некоторые из них экспрессируются в почке постоянно (конституциональные молекулы), а локальный синтез других многократно усиливается под действием воспалительного микроокружения (индуцибельные молекулы). В обзоре обсуждается роль регуляторных иммунных клеток при повреждении почечной ткани, подробно рассмотрены эффекты отдельных факторов самозащиты (противовоспалительных цитокинов, липоксинов, ингибиторов протеолиза, белков теплового шока), представлены результаты их эффективного применения в эксперименте на различных моделях нефрита. Усиление эндогенных защитных механизмов путем введения ключевых факторов, способных модулировать воспаление в почке и «переключать» этот процесс в сторону ограничения/резолюции, представляет собой перспективное направление терапевтического воздействия при прогрессирующих заболеваниях почек у человека.

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Ключевые слова: chronic glomerulonephritis, self-defense mechanism, anti-inlflammatory cytokines, lipotoxins, proteolysis inhibitors, heat shock proteins, хронический гломерулонефрит, механизмы самозащиты, противовоспалительные цитокины, липоксины, ингибиторы протеолиза, белки теплового шока

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