肾脏纤维化是慢性肾脏病（CKD）发展至终末期肾脏疾病（ESRD）的典型病理变化，其特征为肾小球硬化和肾小管间质纤维化。然而，目前有限且昂贵的治疗肾脏纤维化的选择对患者和医疗系统造成沉重的财务负担。因此，寻找一种有效的肾脏纤维化治疗方法具有重要意义。铁死亡（Ferroptosis）作为一种非传统形式的细胞死亡已被发现在急性肾损伤（AKI）、肿瘤、神经退行性疾病等方面发挥重要作用。此外，越来越多的研究表明铁死亡可能是肾脏纤维化的一个潜在靶点。同时，线粒体自噬（mitophagy）是一种选择性自噬，可以选择性降解受损或功能异常的线粒体，作为线粒体质量控制的一种形式，减少产生的活性氧类物质（ROS）的积累，而ROS的积累是导致肾脏纤维化的主要原因。此外，作为线粒体自噬的受体，NIX可以释放beclin1诱导线粒体自噬，还可以结合溶质载体家族7类成员11（SLC7A11），阻断半胱氨酸/谷氨酸抗转运蛋白（系统Xc-）的活性，抑制铁死亡，提示了线粒体自噬和铁死亡之间的联系。然而，关于线粒体自噬、铁死亡和肾脏纤维化之间的关系，目前只有有限的研究。本文将评述线粒体自噬的机制，并描述铁死亡和线粒体自噬与肾脏纤维化的关系，以期发现肾脏纤维化治疗的潜在新靶点。

Renal fibrosis, characterized by glomerulosclerosis and tubulointerstitial fibrosis, is a typical pathological alteration in the progression of chronic kidney disease (CKD) to end-stage renal disease (ESRD). However, the limited and expensive options for treating renal fibrosis place a heavy financial burden on patients and healthcare systems. Therefore, it is significant to find an effective treatment for renal fibrosis. Ferroptosis, a non-traditional form of cell death, has been found to play an important role in acute kidney injury (AKI), tumors, neurodegenerative diseases, and so on. Moreover, a growing body of research suggests that ferroptosis might be a potential target of renal fibrosis. Meanwhile, mitophagy is a type of selective autophagy that can selectively degrade damaged or dysfunctional mitochondria as a form of mitochondrial quality control, reducing the production of reactive oxygen species (ROS), the accumulation of which is the main cause of renal fibrosis. Additionally, as a receptor of mitophagy, NIX can release beclin1 to induce mitophagy, which can also bind to solute carrier family 7 member 11 (SLC7A11) to block the activity of cystine/glutamate antitransporter (system Xc-) and inhibit ferroptosis, thereby suggesting a link between mitophagy and ferroptosis. However, there have been only limited studies on the relationship among mitophagy, ferroptosis and renal fibrosis. In this paper, we review the mechanisms of mitophagy, and describe how ferroptosis and mitophagy are related to renal fibrosis in an effort to identify potential novel targets for the treatment of renal fibrosis.