Uric acid-induced C-reactive protein expression: implication on cell proliferation and nitric oxide production of human vascular cells.
By D. Kang, Sung-Kwang Park, In-kyu Lee, Richard J. Johnson. Journal of the American Society of Nephrology, 2005
913 citations recorded by the source corpus.
Subfields: Molecular Biology, Nephrology
View Paper: https://www.semanticscholar.org/paper/881f7a95269865c6bc92ca3788018d1ea77b3290
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Citations in the corpus
- Uric Acid: The Oxidant-Antioxidant Paradox (2008, neutral): “[49−52] Uric acid induced an activation of protein kinase p38 in adipocytes (Figure 3), as well as in other cell types,[53,54] and our experiments showed that superoxide and active NADPH oxidase were required for this activation”
- Adverse effects of the classic antioxidant uric acid in adipocytes: NADPH oxidase-mediated oxidative/nitrosative stress. (2007, background): “In endothelial cells, uric acid decreases NO bioavailability (27, 30) and inhibits cell migration and proliferation, which are mediated in part by the expression of C-reactive protein (27).”
- Sugar, Uric Acid, and the Etiology of Diabetes and Obesity (2013, background): “Uric acid reduces endothelial NO via several mechanisms, including blocking the uptake of the substrate, L-arginine (47), stimulating the degradation of L-arginine by arginase (48), and scavenging NO by uric acid or by uric acid–generated oxidants (32,34,49).”
- Uric acid and chronic kidney disease: which is chasing which? (2013, background): “RAS, renin–angiotensin system.”
- Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease, and cardiovascular disease. (2007, background): “Uric acid potently reduces the concentrations of endothelial nitric oxide in vitro and in vivo in experimental animals (64, 65).”