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Oxidative Stress and Diabetic Complications
Open accessAbstract
Oxidative stress plays a pivotal role in the development of diabetes complications, both microvascular and cardiovascular. The metabolic abnormalities of diabetes cause mitochondrial superoxide overproduction in endothelial cells of both large and small vessels, as well as in the myocardium. This increased superoxide production causes the activation of 5 major pathways involved in the pathogenesis of complications: polyol pathway flux, increased formation of AGEs (advanced glycation end products), increased expression of the receptor for AGEs and its activating ligands, activation of protein kinase C isoforms, and overactivity of the hexosamine pathway. It also directly inactivates 2 critical antiatherosclerotic enzymes, endothelial nitric oxide synthase and prostacyclin synthase. Through these pathways, increased intracellular reactive oxygen species (ROS) cause defective angiogenesis in response to ischemia, activate a number of proinflammatory pathways, and cause long-lasting epigenetic changes that drive persistent expression of proinflammatory genes after glycemia is normalized (“hyperglycemic memory”). Atherosclerosis and cardiomyopathy in type 2 diabetes are caused in part by pathway-selective insulin resistance, which increases mitochondrial ROS production from free fatty acids and by inactivation of antiatherosclerosis enzymes by ROS. Overexpression of superoxide dismutase in transgenic diabetic mice prevents diabetic retinopathy, nephropathy, and cardiomyopathy. The aim of this review is to highlight advances in understanding the role of metabolite-generated ROS in the development of diabetic complications.
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“Chronic overproduction of ROS increases oxidative stress, damages DNA, increases apoptosis, and triggers inflammation, which is a key feature in T2DM and metabolic syndrome (42).”
From TFAM Enhances Fat Oxidation and Attenuates High-Fat Diet–Induced Insulin Resistance in Skeletal Muscle (2019) · cites this paper as [42]
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“Taken together, our data suggest significant molecular and metabolic perturbations between NHOs and PGDHOs consistent with previous studies on PGD suggesting increased oxidative stress, cardiomyopathy, and altered lipid profiles48–50”
From Self-assembling human heart organoids for the modeling of cardiac development and congenital heart disease (2021) · cites this paper as [49]
In the citing paper
“Hyperglycemia and PKC activation-induced ROS production result in inflammatory changes in the vascular endothelium including monocytes adhesion, formation of foam cells, and activation of major biochemical paths including polyol pathway flux and increased formation of advanced glycation end products, further contributing to the development of atherosclerosis.40”
From Glycemic variability and cardiovascular disease in patients with type 2 diabetes (2021) · cites this paper as [40]
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Metadata
- Authors
- Giacco, F., & Brownlee, M.
- Affiliations
- Albert Einstein College of Medicine (US)
- Corresponding author
- Brownlee, Michael
- Venue
- Circulation Research
- Published
- 2010-10-29
- Volume
- 107
- Issue
- 9
- Pages
- 1058-1070
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- PMC
- PMC2996922
- OpenAlex
- W2105731956
- Cited by
- 5,461
- References
- 152
- Citations by year
- 2026: 305 · 2025: 331 · 2024: 416 · 2023: 448 · 2022: 478 · 2021: 435 · 2020: 411 · 2019: 349 · 2018: 370 · 2017: 367 · 2016: 338 · 2015: 318 · 2014: 327 · 2013: 260 · 2012: 203
- FWCI
- 17.36
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Circulation Research (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK074153, R01-DK07453, P60DK020541)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- oxidative stress, diabetes complications, superoxide, reactive oxygen species, mitochondrial dysfunction, polyol pathway, advanced glycation end products, AGE receptor, protein kinase C, hexosamine biosynthetic pathway, endothelial nitric oxide synthase, prostacyclin synthase, angiogenesis, inflammation, epigenetic modifications, atherosclerosis, diabetic cardiomyopathy, type 2 diabetes, insulin resistance, superoxide dismutase, diabetic retinopathy, diabetic nephropathy
- MeSH terms
- Animals, Humans, Hyperglycemia, Cardiomyopathies, Signal Transduction, Reactive Oxygen Species, Oxidative Stress, Diabetes Complications, Atherosclerosis, Microvessels
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