Although fibrosis is a common pathological feature of most end-stage organ diseases, its pathogenesis remains unclear. There is growing evidence that mitochondrial dysfunction contributes to the development and progression of fibrosis. The heart, liver, kidney and lung are highly oxygen-consuming organs that are sensitive to mitochondrial dysfunction. Moreover, the fibrotic process of skin and islet is closely related to mitochondrial dysfunction as well. This review summarized emerging mechanisms related to mitochondrial dysfunction in different fibrotic organs and tissues above. First, it highlighted the important elucidation of mitochondria morphological changes, mitochondrial membrane potential and structural damage, mitochondrial DNA (mtDNA) damage and reactive oxidative species (ROS) production, etc. Second, it introduced the abnormality of mitophagy and mitochondrial transfer also contributed to the fibrotic process. Therefore, with gaining the increasing knowledge of mitochondrial structure, function, and origin, we could kindle a new era for the diagnostic and therapeutic strategies of many fibrotic diseases based on mitochondrial dysfunction.

尽管纤维化是大多数终末期器官疾病的共同病理特征，但其发病机制仍不清楚。越来越多的证据表明线粒体功能障碍会导致纤维化的发生和进展。心脏、肝脏、肾脏和肺是高耗氧器官，对线粒体功能障碍很敏感。此外，皮肤和胰岛的纤维化过程也与线粒体功能障碍密切相关。本综述总结了上述不同纤维化器官和组织中与线粒体功能障碍相关的新机制。首先，强调了线粒体形态变化、线粒体膜电位和结构损伤、线粒体DNA（mtDNA）损伤和活性氧化物质（ROS）产生等的重要阐明。其次，介绍了线粒体自噬和线粒体转移的异常也有助于线粒体自噬和线粒体转移的发生。纤维化过程。因此，随着对线粒体结构、功能和起源的了解不断增加，我们可以为许多基于线粒体功能障碍的纤维化疾病的诊断和治疗策略开辟一个新时代。