Oxidative Stress and NRF2 in Diabetes

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: 30 September 2025 | Viewed by 1268

Special Issue Editor


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Guest Editor
1. Division of Metabolism, Endocrinology, and Nutrition, University of Washington Seattle, Seattle, WA, USA
2. Metabolism Division, University of Minnesota Medical School, Minneapolis, MN, USA
Interests: pancreas islet; insulin dependent diabetes mellitus; cytokines; endocrinology; diabetes; oxidative stress; Nrf2

Special Issue Information

Dear Colleagues,

Diabetes is a chronic metabolic disorder characterized by elevated blood glucose levels, which can lead to severe complications if not managed properly. One of the critical pathological mechanisms in diabetes is oxidative stress, which arises from an imbalance between the production of reactive oxygen species (ROS) and the body’s ability to detoxify these reactive intermediates through antioxidants.

Oxidative stress is implicated in the progression of both type 1 and type 2 diabetes, contributing to insulin resistance, impaired insulin secretion, and beta-cell dysfunction. It also plays a significant role in the development of diabetes-related complications such as retinopathy, nephropathy, neuropathy, and cardiovascular diseases. NRF2 is a transcription factor that regulates the expression of antioxidant proteins that protect against oxidative damage. In the context of diabetes, activating the NRF2 pathway could potentially restore redox balance, assist beta cell repair, improve insulin sensitivity, and reduce the incidence of complications.

The Special Issue on “Oxidative Stress and NRF2 in Diabetes” aims to bring together research and review articles that delve into the mechanisms by which NRF2 modulates oxidative stress in diabetes and explore therapeutic strategies targeting NRF2 to ameliorate diabetes-related oxidative damage. It will highlight advances in the understanding of how NRF2 can be leveraged to develop novel treatments that improve diabetic outcomes by enhancing the body’s antioxidant defenses.

Dr. R. Paul Robertson
Guest Editor

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Keywords

  • oxidative stress
  • NRF2
  • ROS
  • diabetes
  • diabetes-related complications
  • insulin

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Published Papers (1 paper)

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Review

19 pages, 1420 KiB  
Review
Oxidative Stress Induced by Nuclear Factor Erythroid 2-Related Factor 2 (NRF2) Dysfunction Aggravates Chronic Inflammation Through the NAD+/SIRT3 Axis and Promotes Renal Injury in Diabetes
by Runyuan Li, Xiaoyu Yan, Yuanxin Zhao, Huan Liu, Jian Wang, Yuan Yuan, Qianyuan Li and Jing Su
Antioxidants 2025, 14(3), 267; https://doi.org/10.3390/antiox14030267 - 25 Feb 2025
Viewed by 743
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 [...] Read more.
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. Full article
(This article belongs to the Special Issue Oxidative Stress and NRF2 in Diabetes)
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