Review
doi: 10.5935/abc.20190077.Kidney Disease in Diabetes Mellitus: Cross-Linking between Hyperglycemia, Redox Imbalance and Inflammation
[Article in English, Portuguese]
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- PMID:31188964
- PMCID: PMC6555585
- DOI: 10.5935/abc.20190077
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Review
Kidney Disease in Diabetes Mellitus: Cross-Linking between Hyperglycemia, Redox Imbalance and Inflammation
[Article in English, Portuguese]
Rayne Gomes Amorim et al. Arq Bras Cardiol..
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- Erratum.[No authors listed][No authors listed]Arq Bras Cardiol. 2019 Aug 8;113(1):182. doi: 10.5935/abc.20190133.Arq Bras Cardiol. 2019.PMID:31411302Free PMC article.
Abstract
Chronic hyperglycemia is the key point of macro- and microvascular complications associated with diabetes mellitus. Excess glucose is responsible for inducing redox imbalance and both systemic and intrarenal inflammation, playing a critical role in the pathogenesis of diabetic kidney disease, which is currently the leading cause of dialysis in the world. The pathogenesis of the disease is complex, multifactorial and not fully elucidated; many factors and mechanisms are involved in the development, progression and clinical outcomes of the disease. Despite the disparate mechanisms involved in renal damage related to diabetes mellitus, the metabolic mechanisms involving oxidative/inflammatory pathways are widely accepted. The is clear evidence that a chronic hyperglycemic state triggers oxidative stress and inflammation mediated by altered metabolic pathways in a self-perpetuating cycle, promoting progression of cell injury and of end-stage renal disease. The present study presents an update on metabolic pathways that involve redox imbalance and inflammation induced by chronic exposure to hyperglycemia in the pathogenesis of diabetic kidney disease.
Conflict of interest statement
No potential conflict of interest relevant to this article was reported.
Figures
Oxidative stress and enzymatic antioxidant defense system in diabeticrenal cells. CAT: catalase; ROS: reactive oxygen species; GPx:glutathione peroxidase; GSH: glutathione; GSSG: oxidizedglutathione; RG: reduced glutathione; H2O2:hydrogen peroxide; NRF2: nuclear erythroid 2-related factor 2;O2: molecular oxygen; NOX: NADPH oxidase;O2•-: superoxide anion radical;•OH: hydroxyl radical; SOD: superoxidedismutase. Adapted from Bhargava.
Schematic representation of the pathways preceding glycolysis andinduction of oxidative stress. ETC: electron transport chain;1,3-BPG: bisphosphoglycerate; G6P: glucose 6-phosphate; G3P:glyceraldehyde-3-phosphate; GAPDH: glyceraldehyde-3-phosphatedehydrogenase; F6P: fructose-6-phosphate; F-1,6-P:fructose-1,6-phosphate; PKC: protein kinase C; AGE; advancedglycation end-products
Mediators of kidney injury induced by chronic hyperglycemia via redoximbalance and inflammation in the pathogenesis of diabetic kidneydisease. ROS: reactive oxygen species; ERK: extracellularsignal-related kinases; TNF- α: tumor necrosis factor alpha;NF-κB: nuclear factor-kappa B; VEGF: the vascular endothelialgrowth factor; IL-1: interleukin 1; IL-6: interleukin 6; IL-18:interleukin 18; ECM: extracellular matrix; NOX: NADPH oxidase;-O-GLaNAc: O-glycosylated into N-acetylglucosamine; PAI-1:plasminogen activator inhibitor-1; AGE: advanced glycationend-products; PKC: protein kinase C; MCP-1: monocyte chemotacticprotein-1; RPGA: receptor for advanced glycation end products; RAAS:renin-angiotensin aldosterone system; TGF-β: transforminggrowth factor-beta.
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