Endothelin Antagonism and Interleukin-6 Inhibition Attenuate the Proatherogenic Effects of C-Reactive Protein

By S. Verma, Shu-hong Li, M. Badiwala, R. Weisel, P. Fedak, Ren-Ke Li, B. Dhillon, D. Mickle. Circulation, 2002

677 citations recorded by the source corpus.

Subfields: Epidemiology, Immunology, Oncology

View Paper: https://www.semanticscholar.org/paper/8dc732208669579c32c57ef596420775a6bca313

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In Epidemiology

1. P. Ridker
2. Peter Libby
3. G. Hansson
4. S. Grundy
5. N. Rifai
6. J. Willerson
7. Renu Virmani
8. Erling Falk

In Immunology

1. Peter Libby
2. P. Ridker
3. G. Hansson
4. Erling Falk
5. Renu Virmani
6. S. Grundy
7. Christie M. Ballantyne
8. I. Tabas

In Oncology

1. P. Ridker
2. Peter Libby
3. G. Hansson
4. N. Rifai
5. B. K. Pedersen

Citations in the corpus

• C-reactive protein and the risk of developing hypertension. (2003, background): “Higher levels of C-reactive protein may increase BP by reducing nitric oxide production in endothelial cells,(12,13) resulting in vasoconstriction and increased production of endothelin 1.(14,15) C-reactive protein may also function as a proatherosclerotic factor by upregulating angiotensin type 1 r”
• Mortality in COPD: role of comorbidities (2006, background): “However, in an inflammatory state (such as diabetes, COPD or obesity), the endothelium begins to over express surface adhesion molecules, such as vascular cell adhesion molecule-1, that allow circulating white blood cells to adhere to damaged endothelial surfaces [ 80 , 81].”
• From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: Part II. (2003, background): “In Search of the Vulnerable Patient The ideal method for screening vulnerable patients should be (1) inexpensive, (2) relatively noninvasive, (3) widely reproducible, (4) readily applicable to an asymptomatic population, and (5) capable of adding predicted value to measurements of established risk f”
• From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: Part I. (2003, background): “Although CRP is a nonspecific marker of systemic inflammation, it activates endothelium and accumulates in the plaque, suggesting an important role in plaque inflammation [96, 97].”
• Emerging risk factors for atherosclerotic vascular disease: a critical review of the evidence. (2003, background): “The protein is markedly up-regulated in atheromatous plaques,36 where it may promote low-density lipoprotein (LDL) cholesterol uptake by macrophages, a key step in atherogenesis.37 C-reactive protein may also induce the expression of intercellular adhesion molecules by endothelial cells,38 thereby f”