Oxidative Stress as a Major Culprit in Kidney Disease in Diabetes
Abstract
It is postulated that localized tissue oxidative stress is a key component in the development of diabetic nephropathy. There remains controversy, however, as to whether this is an early link between hyperglycemia and renal disease or develops as a consequence of other primary pathogenic mechanisms. In the kidney, a number of pathways that generate reactive oxygen species (ROS) such as glycolysis, specific defects in the polyol pathway, uncoupling of nitric oxide synthase, xanthine oxidase, NAD(P)H oxidase, and advanced glycation have been identified as potentially major contributors to the pathogenesis of diabetic kidney disease. In addition, a unifying hypothesis has been proposed whereby mitochondrial production of ROS in response to chronic hyperglycemia may be the key initiator for each of these pathogenic pathways. This postulate emphasizes the importance of mitochondrial dysfunction in the progression and development of diabetes complications including nephropathy. A mystery remains, however, as to why antioxidants per se have demonstrated minimal renoprotection in humans despite positive preclinical research findings. It is likely that the utility of current study approaches, such as vitamin use, may not be the ideal antioxidant strategy in human diabetic nephropathy. There is now an increasing body of data to suggest that strategies involving a more targeted antioxidant approach, using agents that penetrate specific cellular compartments, may be the elusive additive therapy required to further optimize renoprotection in diabetes.
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The NOX enzymes together with mitochondrial superoxide represent the most important sources of ROS in diabetes mellitus and diabetic micro-/macro-vascular diseases.
“The NOX enzymes together with mitochondrial superoxide represent the most important sources of ROS in diabetes mellitus and diabetic micro-/macro-vascular diseases (Forbes et al. 2008; Miric et al. 2016).”
From Reactive Oxygen Species, Toxicity, Oxidative Stress, and Antioxidants: Chronic Diseases and Aging (2023) · cites this paper as Forbes et al. 2008
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- Authors
- Forbes, J. M., Coughlan, M. T., & Cooper, M. E.
- Affiliations
- Baker Heart and Diabetes Institute (AU)
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2008-06-01
- Volume
- 57
- Issue
- 6
- Pages
- 1446-1454
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2142693924
- Cited by
- 1,203
- References
- 65
- Citations by year
- 2026: 17 · 2025: 36 · 2024: 50 · 2023: 72 · 2022: 62 · 2021: 67 · 2020: 81 · 2019: 74 · 2018: 77 · 2017: 68 · 2016: 69 · 2015: 78 · 2014: 89 · 2013: 77 · 2012: 83
- FWCI
- 8.95
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Keywords
- oxidative stress, diabetic nephropathy, reactive oxygen species, hyperglycemia, mitochondrial dysfunction, polyol pathway, nitric oxide synthase uncoupling, xanthine oxidase, NADPH oxidase, advanced glycation, antioxidants, renal protection
- MeSH terms
- Animals, Cytosol, Diabetic Nephropathies, Disease Models, Animal, Energy Metabolism, Glucose, Glucosephosphate Dehydrogenase, Glycolysis, Humans, Mitochondria, NAD, Oxidation-Reduction, Oxidative Phosphorylation, Sorbitol, Glycation End Products, Advanced, Reactive Oxygen Species, Oxidative Stress
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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