Metabolic changes and oxidative stress in diabetic kidney disease

Midori Sakashita, Tetsuhiro Tanaka, Reiko Inagi

Research output: Contribution to journalReview articlepeer-review

28 Citations (Scopus)


Diabetic kidney disease (DKD) is a major cause of end-stage kidney disease, and it is crucial to understand the pathophysiology of DKD. The control of blood glucose levels by various glucose-lowering drugs, the common use of inhibitors of the renin–angiotensin system, and the aging of patients with diabetes can alter the disease course of DKD. Moreover, metabolic changes and associated atherosclerosis play a major role in the etiology of DKD. The pathophysiology of DKD is largely attributed to the disruption of various cellular stress responses due to metabolic changes, especially an increase in oxidative stress. Therefore, many antioxidants have been studied as therapeutic agents. Recently, it has been found that NRF2, a master regulator of oxidative stress, plays a major role in the pathogenesis of DKD and bardoxolone methyl, an activator of NRF2, has attracted attention as a drug that increases the estimated glomerular filtration rate in patients with DKD. This review outlines the altered stress responses of cellular organelles in DKD, their involvement in the pathogenesis of DKD, and discusses strategies for developing therapeutic agents, especially bardoxolone methyl.

Original languageEnglish
Article number1143
Issue number7
Publication statusPublished - 2021 Jul


  • Bardoxolone methyl
  • Diabetic kidney disease
  • Nrf2
  • Organelle crosstalk
  • Oxidative stress


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