Mitochondria are organelles that are essential for cellular homeostasis including energy harvesting through oxidative phosphorylation. Mitochondrial dysfunction plays a vital role in liver diseases as it produces a large amount of reactive oxygen species (ROS), in turn leading to further oxidative damage to the structure and function of mitochondria and other cellular components. More severe oxidative damage occurred in mitochondrial DNA (mtDNA) than in nuclear DNA. mtDNA dysfunction results in further oxidative damage as it participates in encoding respiratory chain polypeptides. In addition, mtDNA can leave the mitochondria and enter the cytoplasm and extracellular environment. mtDNA is derived from ancient bacteria, contains many unmethylated CpG dinucleotide repeats similar to bacterial DNA, and thus can induce inflammation to exacerbate damage to liver cells and distal organs by activating toll-like receptor 9, inflammatory bodies, and stimulator of interferon genes (STING). In this review, we focus on the mechanism by which mtDNA alterations cause liver injuries, including nonalcoholic fatty liver, alcoholic liver disease, drug-induced liver injury, viral hepatitis, and liver cancer.

中文翻译：

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线粒体DNA在肝病中氧化应激和炎症激活中的潜在作用

线粒体是细胞动态平衡所必需的细胞器，包括通过氧化磷酸化收集能量。线粒体功能障碍在肝脏疾病中起着至关重要的作用，因为它会产生大量的活性氧（ROS），进而导致线粒体和其他细胞成分的结构和功能发生进一步的氧化损伤。线粒体DNA（mtDNA）中的氧化损伤比核DNA中更严重。mtDNA功能异常会导致进一步的氧化损伤，因为它参与编码呼吸链多肽。另外，mtDNA可以离开线粒体并进入细胞质和细胞外环境。mtDNA源自古代细菌，包含许多与细菌DNA类似的未甲基化的CpG二核苷酸重复序列，因此可以通过激活Toll样受体9，炎性体和干扰素基因的刺激物来诱发炎症，加剧对肝细胞和远端器官的损害。在这篇综述中，我们集中于mtDNA改变引起肝损伤的机制，包括非酒精性脂肪肝，酒精性肝病，药物性肝损伤，病毒性肝炎和肝癌。