The role of mitochondria in systemic lupus erythematosus: A glimpse of various pathogenetic mechanisms.
The role of mitochondria in systemic lupus erythematosus: A glimpse of various pathogenetic mechanisms.
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DOI：
10.2174/0929867326666181126165139
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发表时间：
2020-06
影响因子：
4.1
通讯作者：
Shi-kun Yang;Hao Zhang;Shuaishuai Shi;Ying-qiu Zhu;Na Song;Qing Dai;Wei Zhang;Ming Gui;H. Zhang
中科院分区：
文献类型：
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作者：
Shi-kun Yang;Hao Zhang;Shuaishuai Shi;Ying-qiu Zhu;Na Song;Qing Dai;Wei Zhang;Ming Gui;H. Zhang
背景系统性红斑狼疮（SLE）是一种严重影响人类健康的多系统自身免疫性疾病。各种器官都可能受到影响，包括肾脏或大脑。SLE的传统治疗方法主要依赖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点。方法对已发表的关于SLE线粒体结构和功能异常以及线粒体靶向治疗的文献进行系统检索。结果越来越多的证据表明，线粒体功能障碍在SLE的发病机制中起重要作用，包括影响线粒体DNA损伤、线粒体动力学改变、线粒体生物合成和能量代谢异常、线粒体自噬、氧化应激、炎症反应、细胞凋亡和NETosis等。线粒体的病理生理作用的进一步调查将导致进一步澄清系统性红斑狼疮。特异性狼疮诱导的器官损伤也表现出特征性的线粒体变化。结论对线粒体功能障碍在SLE发病中的作用进行综述，为SLE的治疗提供新的靶点。
BACKGROUND Systemic lupus erythematosus (SLE) is a polysystem autoimmune disease that adversely affects human health. Various organ 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.