Oxidative Stress in Type 2 Diabetes: Impacts from Pathogenesis to Lifestyle Modifications
Open accessAbstract
Oxidative stress is a critical factor in the pathogenesis and progression of diabetes and its associated complications. The imbalance between reactive oxygen species (ROS) production and the body’s antioxidant defence mechanisms leads to cellular damage and dysfunction. In diabetes, chronic hyperglycaemia and mitochondrial dysfunction contribute to increased ROS production, further exacerbating oxidative stress. This oxidative burden adversely affects various aspects of diabetes, including impaired beta-cell function and insulin resistance, leading to disrupted glucose regulation. Additionally, oxidative stress-induced damage to blood vessels and impaired endothelial function contribute to the development of diabetic vascular complications such as retinopathy, nephropathy, and cardiovascular diseases. Moreover, organs and tissues throughout the body, including the kidneys, nerves, and eyes, are vulnerable to oxidative stress, resulting in diabetic nephropathy, neuropathy, and retinopathy. Strategies to mitigate oxidative stress in diabetes include antioxidant therapy, lifestyle modifications, and effective management of hyperglycaemia. However, further research is necessary to comprehensively understand the underlying mechanisms of oxidative stress in diabetes and to evaluate the efficacy of antioxidant interventions in preventing and treating diabetic complications. By addressing oxidative stress, it might be possible to alleviate the burden of diabetes and improve patient outcomes.
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Peroxynitrite oxidizes tetrahydrobiopterin, an essential cofactor for eNOS, rendering it biologically inactive and unable to catalyze endothelial NO synthesis.
“Additionally, peroxynitrite oxidizes tetrahydrobiopterin, an essential cofactor for eNOS, rendering it biologically inactive and unable to catalyze endothelial NO synthesis [15].”
From New Developments in Pharmacological Treatment of Obesity and Type 2 Diabetes—Beyond and within GLP-1 Receptor Agonists (2024) · cites this paper as [15]
Section 3 discusses eNOS in diabetic oxidative stress, and Section 5 mentions eNOS in endothelial ROS production, but neither describes the claimed mechanism. Searches for peroxynitrite, tetrahydrobiopterin, and eNOS uncoupling found no passage saying that peroxynitrite oxidizes the cofactor and prevents endothelial NO synthesis. The retrieved passages provide no page numbers. (LLM, conf=0.73)
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Cited by
Sorted by citations
Sztanek, F., Tóth, L. I., Pető, A., Hernyák, M., Diószegi, Á., & Harangi, M. (2024) · Biomedicines · doi:10.3390/biomedicines12061320 · Cited by 43 · see citing works
“Additionally, peroxynitrite oxidizes tetrahydrobiopterin, an essential cofactor for eNOS, rendering it biologically inactive and unable to catalyze endothelial NO synthesis [15].”
BackgroundDiabetic Gastroparesis: Navigating Pathophysiology and Nutritional Interventions
Caturano, A., Cavallo, M., Nilo, D., Vaudo, G., Russo, V., Galiero, R., Rinaldi, L., Marfella, R., Monda, M., Luca, G., et al. (2024) · Gastrointestinal Disorders · doi:10.3390/gidisord6010016 · Cited by 17 · see citing works
Self-citation
- Authors
- Caturano, A., D’Angelo, M., Mormone, A., Russo, V., Mollica, M. P., Salvatore, T., Galiero, R., Rinaldi, L., Vetrano, E., Marfella, R., Monda, M., Giordano, A., & Sasso, F. C.
- Affiliations
- University of Campania "Luigi Vanvitelli" (IT)
- University of Naples Federico II (IT)
- Temple University (US)
- Corresponding author
- Caturano, Alfredo
- ORCID
- Venue
- Current Issues in Molecular Biology
- Publisher
- MDPI AG
- Published
- 2023-08-12
- Volume
- 45
- Issue
- 8
- Pages
- 6651-6666
- ISSN
- 1467-3037 (ISSN-L)
- 1467-3045
- PMC
- PMC10453126
- OpenAlex
- W4385802398
- Cited by
- 579
- References
- 11
- Citations by year
- 2026: 174 · 2025: 256 · 2024: 129 · 2023: 18 · 2014: 1
- FWCI
- 11.49
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Current Issues in Molecular Biology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Use Siena air (University of Siena) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Archivio Istituzionale della Ricerca - Università degli Studi della Campania "Luigi Vanvitelli" (submittedVersion)
- Archivio Istituzionale della Ricerca - Università degli Studi del Molise (submittedVersion)
- Topics
- Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Keywords
- oxidative stress, type 2 diabetes, reactive oxygen species, antioxidant defense, hyperglycemia, mitochondrial dysfunction, beta-cell dysfunction, insulin resistance, endothelial dysfunction, diabetes complications, diabetic retinopathy, diabetic nephropathy, diabetic neuropathy, antioxidant therapy, lifestyle modification
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