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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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Antioxidative therapies for diabetic kidney disease. Oxidative stress can be improved by downregulating the levels of MDA, ROS, and JNKs, and elevating the expression levels of Nrf2, SOD, NQO1, HO-1, and GSH-Px. MDA: malondialdehyde; JNKs: c-Jun N-terminal kinases; SOD: superoxide dismutase; NQO1: NADPH quinone oxidoreductase; HO-1:heme oxygenase-1; GSH-Px: glutathione peroxidase; AMPK/SIRT1-FoxO1: adenosine monophosphate-activated protein kinase/sirtuin1-forkhead box protein O1; cAMP-PKA: cAMP-protein kinase A; SGLT2i: sodium-glucose co-transporter 2 inhibitor; GLP-1RAs: glucagon-like peptide-1 receptor agonists; BET: bromodomain and extra terminal; C5/C5R: complement component 5/complement component 5 receptor; C1-INH: complement component 1 esterase inhibitor; MASP-2: mannose-binding lectin-associated serine protease-2.