No real therapeutic modality is currently available for Acute kidney injury (AKI) and if any, they are mainly supportive in nature. Therefore, developing a new therapeutic strategy is crucial. Mitochondrial dysfunction proved to be a key contributor to renal tubular cell death during AKI. Thus, replacement or augmentation of damaged mitochondria could be a proper target in AKI treatment. Here, in an animal model of AKI, we auto-transplanted normal mitochondria isolated from healthy muscle cells to injured kidney cells through injection to renal artery. The mitochondria transplantation prevented renal tubular cell death, restored renal function, ameliorated kidney damage, improved regenerative potential of renal tubules, and decreased ischemia/reperfusion-induced apoptosis. Although further studies including clinical trials are required in this regard, our findings suggest a novel therapeutic strategy for treatment of AKI. Improved quality of life of patients suffering from renal failure and decreased morbidity and mortality rates would be the potential advantages of this therapeutic strategy.

中文翻译：

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线粒体移植可改善大鼠缺血/再灌注引起的肾脏损伤。

目前尚无用于急性肾损伤（AKI）的真正治疗方法，如果有的话，它们本质上主要是支持性的。因此，制定新的治疗策略至关重要。线粒体功能障碍被证明是AKI期间肾小管细胞死亡的关键原因。因此，替换或增加受损的线粒体可能是AKI治疗的适当目标。在这里，在AKI的动物模型中，我们通过注射至肾动脉，将从健康肌肉细胞中分离出的正常线粒体自动移植到受损的肾细胞中。线粒体移植可防止肾小管细胞死亡，恢复肾功能，减轻肾脏损害，改善肾小管的再生潜能以及减少缺血/再灌注诱导的细胞凋亡。尽管在这方面需要包括临床试验在内的进一步研究，但我们的发现提出了一种新颖的AKI治疗策略。患有肾衰竭的患者的生活质量的改善以及发病率和死亡率的降低将是该治疗策略的潜在优势。