A detective story for biomedical footprints towards new therapeutic interventions in diabetic nephropathy.
The biochemistry of protein modifications in human disease teaches us a number of lessons as it reveals factors and pathways implicated in the genesis of human pathology. For instance, diabetic renal damage is associated with a variety of stresses, e.g., glycemic stress resulting from hyperglycemia, oxidative stress from reactive oxygen species, carbonyl stress from reactive carbonyl compounds, and nitrosative stress from reactive nitrogen species. Proteins are particularly attractive targets for product analysis. Protein modifications are much more specific and stable biomarkers of the disease than lipids and other metabolites, and thus serve as footprints of biochemical processes. Their quantitative analysis not only facilitates better understanding of the physiopathology but also offers new therapeutic insight. In this review, we delineate oxidative protein modifications existing in diabetic nephropathy and discuss therapeutic perspectives towards the development of new classes of renoprotective agents.
Miyata
Toshio
T
Institute of Medical Sciences, Tokai University, Isehara, Kanagawa.
Kurokawa
Kiyoshi
K
D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000503:physiopathology; D003929:Diabetic Neuropathies / Q000188:drug therapy* / Q000503:physiopathology*; D017127:Glycation End Products, Advanced / Q000037:antagonists & inhibitors; D006146:Guanidines / Q000494:pharmacology; D006801:Humans; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D018384:Oxidative Stress; D012084:Renin-Angiotensin System / Q000502:physiology
D017127:Glycation End Products, Advanced; D006146:Guanidines; D019001:Nitric Oxide Synthase; C004479:pimagedine