Carbonyl stress in the pathogenesis of diabetic nephropathy

Daisuke Suzuki, Toshio Miyata

Research output: Contribution to journalReview articlepeer-review

98 Citations (Scopus)


Diabetic nephropathy is a major chronic complication of diabetes mellitus and an important cause of increased morbidity and mortality in diabetic patients. Although several lines of evidence have suggested that poor glycemic control undoubtedly plays a significant role, the metabolic events responsible for its development are not understood well. Possible mediators of untowards effects of hyperglycemia include the advanced glycation end products (AGEs). AGEs, carboxymethyllysine and pentosidine, whose formation is closely linked to oxidation, accumulate in the characteristic diabetic glomerular lesions, such as the expanded mesangial matrix and nodular lesions, in co-localization with other oxidation-specific protein adducts, such as malondialdehyde-lysine, 4-hydroxynonenal-protein adduct, and acrolein-protein adduct. These five biomarkers are formed under oxidative stress by carbonyl amine chemistry between protein amino group and carbonyl compounds derived from carbohydrates, lipids, and amino acids. This article focuses on new aspects of the pathology of diabetic nephropathy, implicating an increased oxidative stress and carbonyl modification of proteins by autoxidation products of carbohydrates, lipids, and amino acids in diabetic glomerular tissue damage ("carbonyl stress").

Original languageEnglish
Pages (from-to)309-314
Number of pages6
JournalInternal Medicine
Issue number4
Publication statusPublished - 1999 Apr


  • Advanced glycation end products (AGEs)
  • Carbonyl compounds
  • Glycoxidation
  • Oxidation


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