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register hereAcute pancreatitis (AP) is an inflammatory disease of the pancreas and a complex process involving multiple factors, with mitochondrial damage playing a crucial role.Mitochondrial dysfunction is now considered a key driver in the development of AP. This dysfunction often presents as increased oxidative stress, altered membrane potential and permeability, and mitochondrial DNA damage and mutations.

急性胰腺炎（AP）是一种胰腺炎症性疾病，是一个涉及多种因素的复杂过程，线粒体损伤起着至关重要的作用。线粒体功能障碍现在被认为是AP发展的关键驱动因素。这种功能障碍通常表现为氧化应激增加，膜电位和通透性改变以及线粒体DNA损伤和突变。

Under stress conditions, mitochondrial dynamics and mitochondrial ROS production increase, leading to decreased mitochondrial membrane potential, imbalanced calcium homeostasis, and activation of the mitochondrial permeability transition pore. The release of mitochondrial DNA (mtDNA), recognized as damage-associated molecular patterns, can activate the cGAS-STING1 and NF-κB pathway and induce proinflammatory factor expression.

在应激条件下，线粒体动力学和线粒体ROS产生增加，导致线粒体膜电位降低，钙稳态失衡以及线粒体通透性转换孔的激活。线粒体DNA（mtDNA）的释放被认为是与损伤相关的分子模式，可以激活cGAS-STING1和NF-κB途径并诱导促炎因子表达。

Additionally, mtDNA can activate inflammasomes, leading to interleukin release and subsequent tissue damage and inflammation. This review summarizes the relationship between mitochondria and AP and explores mitochondrial protective strategies in the diagnosis and treatment of this disease. Future research on the treatment of acute pancreatitis can benefit from exploring promising avenues such as antioxidants, mitochondrial inhibitors, and new therapies that target mitochondrial dysfunction..

此外，mtDNA可以激活炎性体，导致白细胞介素释放以及随后的组织损伤和炎症。本综述总结了线粒体与AP之间的关系，并探讨了线粒体在该疾病诊断和治疗中的保护策略。未来对急性胰腺炎治疗的研究可以从探索有前途的途径中受益，例如抗氧化剂，线粒体抑制剂以及针对线粒体功能障碍的新疗法。。