Role of oxidative modifications in atherosclerosis.

By R. Stocker, J. Keaney. Physiological Reviews, 2004

2,693 citations recorded by the source corpus.

Subfields: Biochemistry, Immunology, Nutrition and Dietetics

View Paper: https://www.semanticscholar.org/paper/46477df47cfd768740f56b5837ee2e9b3e2c6f4d

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. J. Chapman
2. A. Kontush
3. I. Dalle-Donne
4. A. Milzani
5. K. Griendling
6. R. Rossi
7. R. Colombo
8. E. Niki

In Immunology

1. J. Chapman
2. A. Kontush
3. R. Stocker
4. M. Schwartz
5. Richard J. Johnson
6. K. Griendling
7. Alberico L. Catapano
8. Y. Sautin

In Nutrition and Dietetics

1. J. Chapman
2. A. Kontush
3. J. Keaney

Citations in the corpus

• Lipid peroxidation: mechanisms, inhibition, and biological effects. (2005, result): “Although there is now a consensus that the oxidative modification of LDL is an important initial event in the progression of atherosclerosis and that antioxidants should be effective for prevention of atherosclerosis, the results of many large-scale, long-term intervention studies do not always supp”
• Mechanotransduction in vascular physiology and atherogenesis (2009, background): “Additionally, oxidant stress synergizes with local permeability or retention of lipoproteins, which leads to the generation of oxidized LDL”
• Increased oxidative stress in obesity: implications for metabolic syndrome, diabetes, hypertension, dyslipidemia, atherosclerosis, and cancer. (2013, background): “In response to inflammatory stimulation, endothelial cells produce adhesion molecules, which accelerate the migration of macrophages into the intima [75].”
• Functionally Defective High-Density Lipoprotein: A New Therapeutic Target at the Crossroads of Dyslipidemia, Inflammation, and Atherosclerosis (2006, result): “This mechanism may account, at least in part, for the negative results of recent large-scale placebo-controlled trials that did not show any beneficial effect of low-molecularweight antioxidants, primarily vitamin E, on the development of CV disease (Stocker and Keaney, 2004).”
• Reactive Oxygen Species in Cardiovascular Disease (2011, background): “There is now overwhelming evidence that ROS have a role as second messengers for cellular signal transduction, and the balance between oxidizing and reducing species is known to be an important component of cellular homeostasis (Figure 1) [46, 47].”
• Superoxide Dismutases: Role in Redox Signaling, Vascular Function, and Diseases (2011, neutral): “Third, the amino terminal residues [194–222] contain a C-terminal region corresponding to heparin-binding domain, which has a cluster of positively charged residues and is critical for binding to heparan sulfate proteoglycan.”
• Adverse effects of the classic antioxidant uric acid in adipocytes: NADPH oxidase-mediated oxidative/nitrosative stress. (2007, background): “Albeit there is tremendous complexity of these disorders, an unambiguous common pathogenetic feature for all of them is, paradoxically, an involvement of oxidative stress and oxidative modifications of proteins and lipids as well as redox-dependent low-grade inflammation (5, 13, 18, 53, 57).”
• Combating oxidative stress in vascular disease: NADPH oxidases as therapeutic targets (2011, background): “Oxidative stress not only causes direct and irreversible oxidative damage to macromolecules but also disrupts key redox-dependent signalling processes in the arterial wal”
• Clinical Relevance of Biomarkers of Oxidative Stress (2015, background): “However, oxLDL does not chemically define a specific form of modified LDL, molecule, or family of molecules (166).”