Mechanisms of Increased Vascular Superoxide Production in Human Diabetes Mellitus: Role of NAD(P)H Oxidase and Endothelial Nitric Oxide Synthase

By T. Guzik, S. Mussa, D. Gastaldi, J. Sadowski, C. Ratnatunga, R. Pillai, K. Channon. Circulation, 2002

1,073 citations recorded by the source corpus.

Subfields: Cardiology and Cardiovascular Medicine, Immunology, Physiology

View Paper: https://www.semanticscholar.org/paper/ef1c54b51b72ca219b225d8e65312e600a5c26cd

How researchers see this paper

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In Cardiology and Cardiovascular Medicine

1. Rhian M. Touyz
2. E. Schiffrin
3. A. Shah
4. M. Félétou

In Immunology

1. Rhian M. Touyz
2. E. Schiffrin
3. R. Clempus
4. B. Lassègue
5. A. Shah
6. Jian-Mei Li
7. M. Félétou
8. S. Dikalov

In Physiology

1. Rhian M. Touyz
2. E. Schiffrin
3. R. Clempus
4. A. Shah
5. M. Félétou
6. B. Lassègue
7. Antonio Ceriello
8. J. Petrie

Citations in the corpus

• New insights on oxidative stress and diabetic complications may lead to a "causal" antioxidant therapy. (2003, background): “Superoxide overproduction, when accompanied by increased NO generation, favors the formation of the strong oxidant peroxynitrite (34), which in turn avidly oxidizes tetrahydrobiopterin, an iNOS cofactor, to dihydrobiopterin (35).”
• Endothelial dysfunction - a major mediator of diabetic vascular disease. (2013, background): “Uncoupled eNOS has been shown to contribute to increased superoxide production and endothelial dysfunction in a number of CVD, including coronary artery disease [130] and type 2 diabetes [131].”
• Reactive oxygen species in vascular biology: implications in hypertension (2004, positive): “Gene transfer of GTP cyclohydrolase (GTPCH) I, the enzyme responsible for regenerating BH4, restored arterial GTPCH I activity and BH4 levels, reduced ROS, and improved endotheliumdependent relaxation and NO release in DOCA-salt hypertensive rats, in which endothelial dysfunction results from NAD(P)”
• Endothelial cell superoxide generation: regulation and relevance for cardiovascular pathophysiology. (2004, background): “Endothelial NADPH oxidase activity is increased by 1) mechanical forces such as oscillatory shear stress (67); 2) hypoxia-reoxygenation (77, 136, 141), flow cessation (111), membrane depolarization (4, 140), nutrient deprivation (106), or ischemia (4, 111); 3) G protein-coupled receptor agonists suc”
• Cardiovascular actions of insulin. (2007, background): “In addition, superoxide production and NADPH oxidase expression are significantly higher in internal mammary arteries from individuals with diabetes when compared with matched nondiabetic individuals (397).”
• Vascular NAD(P)H oxidases: specific features, expression, and regulation. (2003, background): “Finally, the mRNAs of the major phagocytic NAD(P)H oxidase subunits p22phox and gp91phox were upregulated in vessels from diabetic animals (80, 91, 94), as well as p22phox, p47phox, and p67phox proteins in vessels from diabetic patients (68).”
• Endothelial dysfunction and vascular disease – a 30th anniversary update (2017, background): “The mechanisms underlying the reduced NO-dependent dilatations in diabetes include: (i) reduced BH4 bioavailability and eNOS uncoupling (Guzik et al. 2002, Pannirselvam et al. 2002, Alp et al. 2003, Cai et al. 2005); (ii) increased activity of arginase, likely resulting from an augmented…”
• Diabetes, Hypertension, and Cardiovascular Disease: Clinical Insights and Vascular Mechanisms (2017, background): “There are some benefits with respect to macrovascular complications, but this is dependent on the profile of individual drug classes and even appears to be different for agents within the same class.88 The role of BP lowering to improve prognosis in T2D has been established since the UK Prospective ”
• Endothelial Dysfunction and Diabetes: Effects on Angiogenesis, Vascular Remodeling, and Wound Healing (2012, background): “eNOS uncoupling and endothelial dysfunction are apparent in experimental models of diabetes and in diabetic patients [77, 84] despite the fact that eNOS expression is actually increased.”