ReviewAntioxidants (Basel, Switzerland)2025
Oxidative Stress Induced by Nuclear Factor Erythroid 2-Related Factor 2 (NRF2) Dysfunction Aggravates Chronic Inflammation Through the NAD
Review in Antioxidants (Basel, Switzerland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- [Effects and mechanisms of broccoli-derived extracellular vesicles on wound healing of full-thickness skin defects in diabetic mice].Zhonghua shao shang yu chuang mian xiu fu za zhi · 2026Article
- Caffeic Acid Counteracts LPS-Induced Inflammatory Damage in Yak Mammary Epithelial Cells Associated with NF-κB-Mediated Autophagy Regulation.Animals : an open access journal from MDPI · 2026Article
- Aspirin Eugenol Ester Alleviates Gastric Injury by Inhibiting Ferroptosis and Oxidative Stress.Antioxidants (Basel, Switzerland) · 2026Article
- Honokiol attenuates diabetic nephropathy by targeting SIRT3 to suppress mitochondrial ROS-induced pyroptosis.Diabetology & metabolic syndrome · 2025Article
- Sulfur-Dependent Disulfide Bond Disruption in Insulin Resistance: A Hypothesis.Advanced pharmaceutical bulletin · 2025Article
- Oxidative Stress, Inflammation, and Cellular Senescence in Neuropathic Pain: Mechanistic Crosstalk.Antioxidants (Basel, Switzerland) · 2025Review
- Total ginsenosides and ginsenoside Rb2 delay hepatocyte senescence by regulating NADJournal of ginseng research · 2025Article
- Association between the total bilirubin to prothrombin time ratio index and diabetic retinopathy, nephropathy, peripheral neuropathy, and foot disease: a retrospective study and risk prediction model construction.Frontiers in endocrinology · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Diabetic nephropathy (DN), one of the most common and severe microvascular complications of diabetes, significantly increases the risk of renal failure and cardiovascular events. A high-glucose environment can lead to mitochondrial dysfunction in macrophages, which, through remodeling of energy metabolism, mediates the polarization of a pro-inflammatory phenotype and contributes to the formation of a chronic inflammatory microenvironment. Recent studies have found that high-glucose stimulation induces dysregulation of the nuclear factor erythroid 2-related factor 2 (NRF2) redox pathway in macrophages, leading to the generation of oxidative stress (OS) that further drives chronic inflammation. Therefore, it is crucial to fully understand how OS affects macrophage phenotypes and functions following NRF2 inhibition. This review analyzes the role of OS induced by NRF2 dysfunction in the chronic inflammation of DN and explores the relationship between OS and macrophage mitochondrial energy metabolism through the NAD⁺/NADH-SIRT3 axis, providing new therapeutic targets for targeting OS to improve the inflammatory microenvironment and vascular damage in DN.
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Registered trials
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