Kidney and Hypertension Section, Joslin Diabetes Center; Beth Israel Deaconess Medical Center, and Harvard Medical School; Joslin Diabetes Center, One Joslin Place, Boston, MA, 02215, USA.
Curr Diab Rep. 2021 Jan 15;21(2):6. doi: 10.1007/s11892-020-01372-2.
Diabetic kidney disease (DKD) continues to be the primary cause of chronic kidney disease in the USA and around the world. The numbers of people with DKD also continue to rise despite current treatments. Certain newer hypoglycemic drugs offer a promise of slowing progression, but it remains to be seen how effective these will be over time. Thus, continued exploration of the mechanisms underlying the development and progression of DKD is essential in order to discover new treatments. Hyperglycemia is the main cause of the cellular damage seen in DKD. But, exactly how hyperglycemia leads to the activation of processes that are ultimately deleterious is incompletely understood.
Studies primarily over the past 10 years have provided novel insights into the interplay of hyperglycemia, glucose metabolic pathways, mitochondrial function, and the potential importance of what has been called the Warburg effect on the development and progression of DKD. This review will provide a brief overview of glucose metabolism and the hypotheses concerning the pathogenesis of DKD and then discuss in more detail the supporting data that indicate a role for the interplay of glucose metabolic pathways and mitochondrial function.
糖尿病肾病（DKD）仍然是美国和世界各地慢性肾脏病的主要病因。尽管目前有治疗方法，但 DKD 患者的数量仍在持续增加。某些新型降糖药物有望减缓疾病进展，但这些药物的长期疗效仍有待观察。因此，为了发现新的治疗方法，探索 DKD 发生和进展的机制至关重要。高血糖是 DKD 中细胞损伤的主要原因。但是，高血糖如何导致最终有害的过程激活尚不完全清楚。
过去 10 年来的研究主要提供了关于高血糖、葡萄糖代谢途径、线粒体功能以及所谓的糖酵解作用对 DKD 发生和进展的潜在重要性之间相互作用的新见解。这篇综述将简要概述葡萄糖代谢以及 DKD 发病机制的假说，然后更详细地讨论表明葡萄糖代谢途径和线粒体功能相互作用发挥作用的支持数据。
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