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糖尿病肾病中的线粒体功能障碍

Mitochondrial Dysfunction in the Diabetic Kidney.

作者信息

Sharma Kumar

机构信息

Institute of Metabolomic Medicine, Center for Renal Translational Medicine, University of California San Diego/Veterans Affairs San Diego Healthcare System, Stein Clinical Research Building, 4th Floor, 9500 Gilman Drive, La Jolla, CA, 92093-0711, USA.

Division of Nephrology-Hypertension, Veterans Affairs San Diego Healthcare System, La Jolla, CA, 92093, USA.

出版信息

Adv Exp Med Biol. 2017;982:553-562. doi: 10.1007/978-3-319-55330-6_28.

Abstract

The role of mitochondria in diabetic complications has been viewed as a source of excess superoxide production leading to cell dysfunction. However, with the lack of benefit of non-specific anti-oxidant approaches this view needs to be re-evaluated. With recent studies using real-time imaging of superoxide, metabolomics, flux studies, transcriptomics and proteomics a new appreciation for the role of mitochondria in the evolution of diabetic kidney disease has emerged. Ongoing studies to further unravel the time course and mechanisms that reduce mitochondrial function will be relevant to novel therapies that could have a major impact on diabetic kidney disease and other diabetic complications.

摘要

线粒体在糖尿病并发症中的作用一直被视为过量产生超氧化物的来源,进而导致细胞功能障碍。然而,由于非特异性抗氧化方法未显示出益处,这一观点需要重新评估。随着最近利用超氧化物实时成像、代谢组学、通量研究、转录组学和蛋白质组学进行的研究,人们对线粒体在糖尿病肾病发展过程中的作用有了新的认识。正在进行的进一步揭示线粒体功能降低的时间进程和机制的研究,将与可能对糖尿病肾病和其他糖尿病并发症产生重大影响的新疗法相关。

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