Клеточный метаболизм и дисфункция митохондрий при хронической обструктивной болезни легких

Хроническая обструктивная болезнь легких (ХОБЛ) в силу многообразия и системности проявлений рассматривается в качестве типичной модели ускоренного старения. К ведущему фактору тканевого ремоделирования при ХОБЛ относятся изменение клеточного метаболизма или его перепрограммирование в ответ на воздействие таких внешних факторов, как продукты сгорания табака, биотопливо, вирусы и др. Среди многообразия механизмов тканевого и клеточного перепрограммирования при ХОБЛ доминирующую позицию занимают вопросы митоходриальной биологии. Являясь парасимбиотическими органеллами, митохондрии имеют сложную систему взаимодействия с клетками целостного организма и участвуют в процессах как биогенеза, или образования новых органелл, так и митофагии, или удаления клеткой-хозяином дефектных митохондрий. При ХОБЛ происходит дизрегуляция обоих этих механизмов.

Целью обзора явилось объединение накопленного научно-исследовательского опыта в области изучения клеточного метаболизма и роли митохондрий для углубленного фенотипирования ХОБЛ в зависимости от вариантов метаболического перепрограммирования и создания новых терапевтических возможностей для их коррекции.

Заключение. Митохондрии являются ключевыми регуляторами метаболизма, окислительно-восстановительного гомеостаза, выживания и пролиферации клеток. Указанные процессы, контролируемые разнообразными путями внутри- и межклеточного сигналинга, демонстрируют дисбаланс при ХОБЛ на уровне различных тканевых дифферонов: альвеолоцитов, эпителиальных клеток легочной ткани, гладких миоцитов дыхательных путей, альвеолярных макрофагов, поперечнополосатой мускулатуры, мезенхимальных стромальных клеток, прогениторных клеток и пр. Результаты, полученные при изучении метаболома и митохондриальной функции, формируют идеи для поиска новых терапевтических возможностей в терапии ХОБЛ.

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