Li Jia, Liu Wenqin, Zhang Jie, Sun Chao
Department of Gastroenterology and Hepatology, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052, China.
Department of Gastroenterology, Tianjin Medical University General Hospital Airport Hospital, East Street 6, Tianjin Airport Economic Area, Tianjin 300308, China.
Int J Biol Sci. 2025 Feb 10;21(4):1767-1783. doi: 10.7150/ijbs.107777. eCollection 2025.
The liver is a vital metabolic organ that detoxifies substances, produces bile, stores nutrients, and regulates versatile metabolic processes. Maintaining normal liver cell function requires the prompt and delicate modulation of mitochondrial quality control (MQC), which encompasses a spectrum of processes such as mitochondrial fission, fusion, biogenesis, and mitophagy. Recent studies have shown that disruptions to this homeostatic status are closely linked to the advent and progression of a variety of acute and chronic liver diseases, including but not limited to alcohol-associated liver disease and metabolic dysfunction-associated fatty liver disease. However, the explicit mechanisms by which mitochondrial dysfunction impacts inflammatory pathways and cell death in the context of liver diseases remain unclear. In this narrative review, we provide a detailed description of MQC, analyze the mechanisms underpinning mitochondrial dysfunction induced by different detrimental insults, and further elucidate how imbalanced/disrupted MQC promotes the progression and aggravation of liver diseases, ultimately shedding light on the mitochondrion-centric therapeutic strategies for these pathophysiological entities.
肝脏是一个重要的代谢器官，具有解毒、产生胆汁、储存营养物质以及调节多种代谢过程的功能。维持正常的肝细胞功能需要线粒体质量控制（MQC）迅速而精细的调节，线粒体质量控制涵盖了一系列过程，如线粒体分裂、融合、生物发生和线粒体自噬。最近的研究表明，这种稳态的破坏与包括但不限于酒精性肝病和代谢功能障碍相关脂肪性肝病在内的各种急慢性肝病的发生和发展密切相关。然而，在肝脏疾病背景下，线粒体功能障碍影响炎症途径和细胞死亡的具体机制仍不清楚。在这篇叙述性综述中，我们详细描述了线粒体质量控制，分析了不同有害损伤诱导线粒体功能障碍的机制，并进一步阐明了失衡/紊乱的线粒体质量控制如何促进肝脏疾病的进展和加重，最终揭示针对这些病理生理实体的以线粒体为中心的治疗策略。
