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. 2024 Apr 12;13(4):455. doi: 10.3390/antiox13040455

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© 2024 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Pathogenesis of diabetic kidney disease (DKD) with oxidative stress. G6P: glucose-6-phosphate; UDP-GlcNAc: uridine diphosphate N-acetylglucosamine; AGEs: receptor for advanced glycation end products; RAGEs: receptor for advanced glycation end products; LOX1: lipoxygenase 1; LDL: low-density lipoprotein; TLR4: toll-like receptor 4; FFAs: free fatty acids; PI3K/Akt: phosphoinositide 3-kinase/protein kinase B; TGF-β/p38-MAPK: transforming growth factor beta/p38-mitogen-activated protein kinase; NF-κB: nuclear factor kappa B; Nrf2/AREs: nuclear factor erythroid 2-related factor 2/antioxidant response elements; JAK/STAT: Janus kinase/signal transducer and activator of transcription; AMPK: adenosine monophosphate-activated protein kinase. These reactions promote inflammation, fibrosis, and apoptosis, ultimately intensifying the progression of DKD.