Background: Systemic Lupus Erythematosus (SLE) is a polysystem autoimmune disease that adversely affects human health. Various organs can be affected, including the kidney or brain. Traditional treatment methods for SLE primarily rely on glucocorticoids and immunosuppressors. Unfortunately, these therapeutic agents cannot prevent a high recurrence rate after SLE remission. Therefore, novel therapeutic targets are urgently required.

Methods: A systematic search of the published literature regarding the abnormal structure and function of mitochondria in SLE and therapies targeting mitochondria was performed in several databases.

Results: Accumulating evidence indicates that mitochondrial dysfunction plays important roles in the pathogenesis of SLE, including influencing mitochondrial DNA damage, mitochondrial dynamics change, abnormal mitochondrial biogenesis and energy metabolism, mitophagy, oxidative stress, inflammatory reactions, apoptosis and NETosis. Further investigation of mitochondrial pathophysiological roles will result in further clarification of SLE. Specific lupus-induced organ damage also exhibits characteristic mitochondrial changes.

Conclusion: This review aimed to summarize the current research on the role of mitochondrial dysfunction in SLE, which will necessarily provide potential novel therapeutic targets for SLE.

背景：系统性红斑狼疮（SLE）是一种多系统自身免疫性疾病，会对人体健康产生不利影响。各种器官都会受到影响，包括肾脏或大脑。SLE的传统治疗方法主要依靠糖皮质激素和免疫抑制剂。不幸的是，这些治疗剂不能防止SLE缓解后的高复发率。因此，迫切需要新的治疗靶标。

方法：在一些数据库中，系统地检索了有关SLE中线粒体的异常结构和功能以及针对线粒体的疗法的已发表文献。

结果：越来越多的证据表明，线粒体功能障碍在SLE的发病机理中起着重要作用，包括影响线粒体DNA损伤，线粒体动力学变化，线粒体生物发生和能量代谢异常，线粒体，氧化应激，炎症反应，细胞凋亡和NETosis。线粒体病理生理作用的进一步研究将进一步澄清SLE。狼疮引起的特定器官损伤也表现出特征性的线粒体变化。

结论：本综述旨在总结当前关于线粒体功能障碍在SLE中的作用的研究，这必将为SLE提供潜在的新治疗靶点。