Hyperglycemia inhibits endothelial nitric oxide synthase activity by posttranslational modification at the Akt site.

By Xue-liang Du, D. Edelstein, Stefanie Dimmeler, Qida Ju, Cheng-fei Sui, M. Brownlee. Journal of Clinical Investigation, 2001

933 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/c286b3386d094acc3c9cfec40d95e493499fda3c

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

1. Gerald W. Hart

In Molecular Biology

1. Gerald W. Hart
2. M. Brownlee
3. Antonio Ceriello
4. L. Rossetti
5. C. Kevil
6. S. Bir
7. G. Kolluru
8. P. Scherer

In Physiology

1. M. Brownlee
2. Gerald W. Hart
3. Antonio Ceriello
4. M. Quon
5. P. Scherer
6. H. Fang
7. R. L. Judd

Citations in the corpus

• New insights into oxidative stress and inflammation during diabetes mellitus-accelerated atherosclerosis (2018, background): “Hyperglycemia, ox-LDL, ROS, BH4 deficiency, L-arginine (an eNOS substrate) and eNOS S-glutathionylation, all lead to the uncoupling of eNOS [121,122].”
• Cardiovascular actions of insulin. (2007, background): “In endothelial cells exposed to high glucose concentrations, insulin-stimulated activation of Akt and eNOS is significantly reduced (240, 241).”
• Inhibition of GAPDH activity by poly(ADP-ribose) polymerase activates three major pathways of hyperglycemic damage in endothelial cells. (2003, background): “Although PKC activation has been implicated in diabetic myocardial dysfunction (41), and both PKC and the hexosamine pathway have been implicated in hyperglycemiainduced loss of endothelium-dependent vasodilatation (42, 43), a possible link between PARP inhibition and activity of these pathways has ”
• Copper, oxidative stress, and human health. (2005, background): “, 2000) as diabetes can result in chronic impairment of eNOS activity (Du et al., 2001).”
• Endothelial Dysfunction and Diabetes: Effects on Angiogenesis, Vascular Remodeling, and Wound Healing (2012, background): “Studies also show that there is an influence of posttranslational modifications leading to decreased eNOS activity under diabetes [107, 125].”
• The endothelial glycocalyx: composition, functions, and visualization (2007, background): “One of the hallmarks of diabetes is insulin absence or resistance and subsequent hyperglycemia, impairing the protective capacity of the vessel wall [73], and resulting in enhanced endothelial permeability [1] and impaired NO synthase function [20].”
• The pathobiology of diabetic complications: a unifying mechanism. (2005, background): “How do we know that this really happens in cells known to be damaged by hyperglycemia? First, we looked at such cells with a dye that changes color with increasing voltage of the mitochondrial membrane and found that intracellular hyperglycemia did indeed increase the voltage across the mitochondria”
• New insights on oxidative stress and diabetic complications may lead to a "causal" antioxidant therapy. (2003, background): “iNOS is induced de novo by various stimuli, including hyperglycemia (29), while the mitochondrial-generated superoxide can inhibit eNOS, although enough NO is still produced (30).”
• Cross Talk Between O-GlcNAcylation and Phosphorylation: Roles in Signaling, Transcription, and Chronic Disease (2011, background): “Many proteins are reciprocally modified under different conditions at the same site by either O-GlcNAc or phosphate, such as at sites on the c-Myc oncogene protein (116), estrogen receptor β (117), some sites on RNA polymerase II (118, 119), endothelial nitric oxide synthase (120), and many others.”