Drug-induced liver injury (DILI) caused by the ingestion of medications, herbs, chemicals or dietary supplements, is a clinically widespread health problem. The underlying mechanism of DILI is the formation of reactive metabolites, which trigger mitochondrial oxidative stress and the opening of mitochondrial permeability transition (MPT) pores through direct toxicity or immune response, leading to cell inflammation, apoptosis, and necrosis. Traditionally, mitochondria play an indispensable role in maintaining the physiological and biochemical functions of cells by producing ATP and mediating intracellular signal transduction; drugs can typically stimulate the mitochondria and, in the case of sustained stress, can eventually cause impairment of mitochondrial function and metabolic activity. Meanwhile, the mitochondrial stress response, as an adaptive protective mechanism, occurs when mitochondrial homeostasis is threatened. In this review, we summarize the relevant frontier researches of the protective effects of mitochondrial stress response in DILI as well as the potential related mechanisms, thus providing some thoughts for the clinical treatment of DILI.

由摄入药物、草药、化学品或膳食补充剂引起的药物性肝损伤 (DILI) 是临床上普遍存在的健康问题。DILI的潜在机制是反应性代谢物的形成，通过直接毒性或免疫反应触发线粒体氧化应激和线粒体通透性转换（MPT）孔的开放，导致细胞炎症、凋亡和坏死。传统上，线粒体通过产生ATP和介导细胞内信号转导，在维持细胞生理生化功能方面发挥着不可或缺的作用；药物通常可以刺激线粒体，在持续压力的情况下，最终会导致线粒体功能和代谢活动受损。同时，线粒体应激反应，作为一种适应性保护机制，当线粒体稳态受到威胁时就会发生。本文综述了线粒体应激反应对DILI保护作用的相关前沿研究以及可能的相关机制，为临床治疗DILI提供一些思路。