High glucose level and free fatty acid stimulate reactive oxygen species production through protein kinase C--dependent activation of NAD(P)H oxidase in cultured vascular cells.

By T. Inoguchi, Ping Li, F. Umeda, Hai-Yan Yu, M. Kakimoto, M. Imamura, Tsuyoshi Aoki, T. Etoh, T. Hashimoto, M. Naruse and 3 more. Diabetes, 2000

1,653 citations recorded by the source corpus.

Subfields: Biochemistry, Biophysics, Physiology

View Paper: https://www.semanticscholar.org/paper/4095276d2da69ab13eefbd93161dcd369f861f63

How researchers see this paper

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

In Biochemistry

1. E. Motz
2. Sushil Kumar Jain
3. A. Shah
4. Prasenjit Manna
5. Jian-Mei Li
6. R. Clempus
7. B. Lassègue

In Physiology

1. R. Clempus
2. Antonio Ceriello
3. A. Shah
4. B. Lassègue
5. G. Boden
6. Sushil Kumar Jain
7. G. King
8. M. Quon

Citations in the corpus

• Cardiac Metabolism in Heart Failure - Implications beyond ATP production (2013, neutral): “Studies in various tissues have linked FA use to increased ROS levels.(96,97) In diabetic cardiomyopathy, ROS have also been associated with myocardial lipid accumulation, lipotoxicity, and decreased cardiac efficiency on the basis of mitochondrial uncoupling.”
• Endothelial dysfunction - a major mediator of diabetic vascular disease. (2013, background): “FFAs have been shown to induce ROS production in the vasculature via mitochondrial uncoupling and by increasing the expression and protein content of NADPH oxidases [75,94].”
• Cardiovascular actions of insulin. (2007, background): “In addition, PKC-dependent activation of NADPH oxidase has been demonstrated in endothelial and VSMCs exposed to FFA (213).”
• Obesity, Oxidative Stress, Adipose Tissue Dysfunction, and the Associated Health Risks: Causes and Therapeutic Strategies (2015, background): “FFA stimulate the production of reactive intermediates through PKC-dependent activation of NOX in cultured vascular cells.(44) Conjugated fatty acids are susceptible to oxidation, stimulate the formation of radicals, and enhance the accumulation of oxidative by-products.”
• NADPH Oxidases in Cardiovascular Health and Disease (2006, neutral): “Both fibrosis and remodeling are therefore markedly influenced by the balance between collagen deposition and matrix degradation, the latter being modulated largely by the activity of MMPs and TIMPS (16).”
• American Association of Clinical Endocrinologists medical guidelines for clinical practice for the management of diabetes mellitus. (2007, neutral): “Initiate combination therapy when HbA1c levels are 7%-8% Options include: Secretagogue + metformin (16,17) Secretagogue + thiazolidinedione (18,19) Secretagogue + α-glucosidase inhibitor (20) Thiazolidinedione + metformin (21,22) Dipeptidyl-peptidase 4 inhibitor + metformin (23) Dipeptidyl-peptidase”
• Endothelial cell superoxide generation: regulation and relevance for cardiovascular pathophysiology. (2004, background): “These include hyperinsulinemia (76), elevated blood glucose and free fatty acids (34, 69), hypercholesterolemia (133, 144, 148), increased AGEs (164, 177), and increased activation of the renin-angiotensin system (98, 176).”
• Diabetes associated cell stress and dysfunction: role of mitochondrial and non‐mitochondrial ROS production and activity (2007, background): “Enzyme activation is initiated by phosphorylation of several serine or threonine residues of the p47phox subunit, mainly by PKC, promoting the subsequent translocation of the cytosolic subunits to the membrane (Inoguchi et al. 2000; Babior, 2002; Fontayne et al. 2002; Bey et al. 2004).”
• Nox family NADPH oxidases: Molecular mechanisms of activation. (2014, background): “For neutrophils it was suggested that TLR4mediates activation of the interleukin-1 receptor-associated kinase-4 (IRAK-4) which phosphorylates p47phox in a PKC- and MAP kinaseindependent manner acting mainly on p47phox Thr133, Ser288, and Thr356 [197].”
• Obesity and Free Fatty Acids (FFA) (2008, background): “FFA-induced insulin resistance also reduces endothelial production of NO through PKC-dependent activation of NAD(P)H oxidase, resulting in increased production of ROS (see the section ‘‘Mechanisms of free fatty acid–mediated insulin resistance’’ and Ref.”