Obstructive nephropathy favors the progression to chronic kidney disease (CKD), a severe health problem worldwide. The unilateral ureteral obstruction (UUO) model is used to study the development of fibrosis. Impairment of renal mitochondria plays a crucial role in several types of CKD and has been strongly related to fibrosis onset. Nevertheless, in the UUO model, the impairment of mitochondria, their relationship with endoplasmic reticulum (ER) stress induction and the participation of both to induce the fibrotic process remain unclear. In this review, we summarize the current information about mitochondrial bioenergetics, redox dynamics, mitochondrial mass, and biogenesis alterations, as well as the relationship of these mitochondrial alterations with ER stress and their participation in fibrotic processes in UUO models. Early after obstruction, there is metabolic reprogramming related to mitochondrial fatty acid β‐oxidation impairment, triggering lipid deposition, oxidative stress, (calcium) Ca²⁺ dysregulation, and a reduction in mitochondrial mass and biogenesis. Mitochondria and the ER establish a pathological feedback loop that promotes the impairment of both organelles by ER stress pathways and Ca²⁺ levels dysregulation. Preserving mitochondrial and ER function can prevent or at least delay the fibrotic process and loss of renal function. However, deeper understanding is still necessary for future clinically‐useful therapies.

中文翻译：

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线粒体功能障碍和内质网应激促进单侧输尿管梗阻所致梗阻性肾病纤维化。

梗阻性肾病有利于发展为慢性肾病 (CKD)，这是全球严重的健康问题。单侧输尿管梗阻 (UUO) 模型用于研究纤维化的发展。肾线粒体受损在几种类型的 CKD 中起着至关重要的作用，并且与纤维化发作密切相关。然而，在 UUO 模型中，线粒体的损​​伤、它们与内质网 (ER) 应激诱导的关系以及两者参与诱导纤维化过程仍不清楚。在这篇综述中，我们总结了有关线粒体生物能学、氧化还原动力学、线粒体质量和生物发生改变的当前信息，以及这些线粒体改变与 ER 应激的关系及其在 UUO 模型中参与纤维化过程的关系。阻塞后早期，²⁺失调，以及线粒体质量和生物发生减少。线粒体和内质网建立病理反馈回路，通过内质网应激途径和 Ca ²⁺水平失调促进两种细胞器的损伤。保留线粒体和 ER 功能可以预防或至少延迟纤维化过程和肾功能丧失。然而，对于未来的临床有用的治疗方法，仍然需要更深入的了解。