Mitochondrial oxidant damage, including damage to mitochondrial DNA (mtDNA) is a feature of both severe microbial infections and inflammation arising from sterile (non-infectious) sources such as tissue trauma. Damaged mitochondria release intact or oxidized fragments of mtDNA into the cytoplasm, which represent oxidant injury, and the fragments promote a spontaneous innate immune response, exemplifying a modern frontier of immunological research. MtDNA and mitochondrial-derived oxidants are central factors in activating at least three innate immune pathways involving the TLR9 (Toll-like receptor 9), the NLRP3 (NACHT, LRR and PYD domains-containing protein-3) inflammasome, and the cGAS (cyclic AMP-GMP synthase) pathway. The events that allow mtDNA to escape from damaged mitochondria and from damaged cells are incompletely known, but the presence of cytoplasmic mtDNA and cell-free mtDNA as immune regulators are important for understanding the cell's capacity for protecting mitochondrial quality control (MQC) and cell viability during inflammatory states.

中文翻译：

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线粒体DNA，氧化剂和先天免疫。

线粒体氧化剂的损害，包括线粒体DNA（mtDNA）的损害，都是严重的微生物感染和由无菌（非传染性）来源（例如组织创伤）引起的炎症的特征。受损的线粒体将完整的或氧化的mtDNA片段释放到细胞质中，这代表了氧化剂的损伤，并且这些片段促进了自发的先天免疫反应，这是免疫学研究的一个现代前沿。MtDNA和线粒体衍生的氧化剂是激活至少三个先天免疫途径的主要因素，这些途径涉及TLR9（Toll样受体9），NLRP3（NACHT，LRR和PYD结构域，含有蛋白3）炎性小体和cGAS（环状AMP-GMP合酶）途径。导致mtDNA从受损的线粒体和受损细胞中逸出的事件尚不完全清楚，