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. 2019 May;112(5):577–587. doi: 10.5935/abc.20190077

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This is an Open Access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Mediators of kidney injury induced by chronic hyperglycemia via redox imbalance and inflammation in the pathogenesis of diabetic kidney disease. ROS: reactive oxygen species; ERK: extracellular signal-related kinases; TNF- α: tumor necrosis factor alpha; NF-κB: nuclear factor-kappa B; VEGF: the vascular endothelial growth 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 glycation end-products; PKC: protein kinase C; MCP-1: monocyte chemotactic protein-1; RPGA: receptor for advanced glycation end products; RAAS: renin-angiotensin aldosterone system; TGF-β: transforming growth factor-beta.