Li Ying, Hepokoski Mark, Gu Wanjun, Simonson Tatum, Singh Prabhleen
Division of Nephrology and Hypertension, University of California San Diego, San Diego, CA 92093, USA.
VA San Diego Healthcare System, San Diego, CA 92161, USA.
J Clin Med. 2021 Sep 3;10(17):3991. doi: 10.3390/jcm10173991.
Acute kidney injury (AKI) significantly contributes to morbidity and mortality in critically ill patients. AKI is also an independent risk factor for the development and progression of chronic kidney disease. Effective therapeutic strategies for AKI are limited, but emerging evidence indicates a prominent role of mitochondrial dysfunction and altered tubular metabolism in the pathogenesis of AKI. Therefore, a comprehensive, mechanistic understanding of mitochondrial function and renal metabolism in AKI may lead to the development of novel therapies in AKI. In this review, we provide an overview of current state of research on the role of mitochondria and tubular metabolism in AKI from both pre-clinical and clinical studies. We also highlight current therapeutic strategies which target mitochondrial function and metabolic pathways for the treatment of AKI.
急性肾损伤(AKI)显著增加了危重症患者的发病率和死亡率。AKI也是慢性肾脏病发生和进展的独立危险因素。针对AKI的有效治疗策略有限,但新出现的证据表明,线粒体功能障碍和肾小管代谢改变在AKI发病机制中起重要作用。因此,全面、深入地了解AKI中线粒体功能和肾脏代谢可能会带来AKI新疗法的研发。在本综述中,我们从临床前和临床研究两方面概述了目前关于线粒体和肾小管代谢在AKI中作用的研究现状。我们还重点介绍了目前针对线粒体功能和代谢途径治疗AKI的治疗策略。