Review explores mechanisms and interventions of mitochondrial autophagy in sepsis-related acute kidney injury, highlighting treatment implications.
脓毒症相关急性肾损伤(sa-Aki)是icu常见的严重并发症,线粒体功能障碍在其发生发展中发挥关键作用。线粒体自噬作为线粒体质量控制的核心机制,通过清除受损线粒体、抑制活性氧积累与炎症信号激活,对肾小管上皮细胞具有重要保护效应。本文就sa-Aki中线粒体自噬的主要分子通路、调控机制及靶向干预策略进行综述,以期为该领域基础研究与临床转化提供参考。
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李 et al. (2026) studied this question.
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