Mitochondrial quality control in acute liver injury and its therapeutic implications (Review)

Abstract

Acute liver injury (ALI) is a clinically important syndrome with limited mechanism-based therapies. Notably, mitochondrial dysfunction is increasingly recognized as a central driver of hepatocellular damage and repair failure. The present narrative review aims to summarize the current evidence on mitochondrial quality control (MQC) in ALI, with an emphasis on mitophagy, mitochondrial biogenesis, mitochondrial dynamics, etiology-specific regulation and therapeutic implications. For the present review, relevant experimental and translational studies addressing MQC-related mechanisms and interventions in major forms of ALI, including drug-induced liver injury, ischemia-reperfusion injury and viral ALI, were reviewed and integrated. The findings indicated that MQC operates as an interconnected network rather than as isolated pathways. Mitophagy, mitochondrial dynamics and mitochondrial biogenesis are temporally coordinated to remove damaged mitochondria, remodel mitochondrial networks and restore bioenergetic capacity. However, MQC responses differ across ALI etiologies, and inappropriate or excessive activation may become maladaptive. In conclusion, understanding MQC as a dynamic and context-dependent repair system may provide a conceptual basis for precision interventions in ALI. Future studies should clarify spatiotemporal MQC regulation, establish reliable biomarkers and validate MQC-targeted therapies in clinically relevant settings.