Cited by 5,461Nitric Oxide and Endothelin EffectsAdvanced Glycation End Products researchRedox biology and oxidative stress

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Oxidative Stress and Diabetic Complications

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Giacco, Ferdinando, Brownlee, Michael·2010·Circulation Research

DOI 10.1161/circresaha.110.223545PMC PMC2996922

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Abstract

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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Authors: Giacco, F., & Brownlee, M.
Affiliations: Albert Einstein College of Medicine (US)
Corresponding author: Brownlee, Michael
Venue: Circulation Research
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 2010-10-29
Volume: 107
Issue: 9
Pages: 1058-1070
ISSN: 0009-7330 (ISSN-L)
1524-4571
DOI: 10.1161/circresaha.110.223545
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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