Generation of C-reactive protein and complement components in atherosclerotic plaques.

By K. Yasojima, C. Schwab, E. Mcgeer, P. Mcgeer. American Journal of Pathology, 2001

627 citations recorded by the source corpus.

Subfields: Cancer Research, Epidemiology, Immunology

View Paper: https://www.semanticscholar.org/paper/bb62e142e645013fd8f7efb03c0ff220c574eca4

How researchers see this paper

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

In Cancer Research

1. P. E. Van den Steen
2. J. Vandooren
3. G. Opdenakker
4. Christopher K. Glass

In Epidemiology

1. Christopher K. Glass
2. P. Calder
3. I. Tabas
4. K. Moore

In Immunology

1. Christopher K. Glass
2. Andrew C. Li
3. P. Calder
4. I. Tabas
5. K. Moore

Citations in the corpus

• Biochemistry and molecular biology of gelatinase B or matrix metalloproteinase-9 (MMP-9): The next decade (2013, background): “In atherosclerotic plaques, complement components are upregulated (Yasojima et al., 2001) and the complement component C5a induces mRNA levels of MMP-1 and MMP-9 in human macrophages (Speidl et al., 2011).”
• The macrophage foam cell as a target for therapeutic intervention (2002, background): “Although CRP is produced mainly in the liver, CRP mRNA and protein can be found in macrophages and smooth muscle cells of human atherosclerotic lesion”
• Innate and acquired immunity in atherogenesis (2002, background): “CRP may be involved in atherogenesis, however, as indicated by the observation that it is secreted by intimal macrophages, as discussed belo”
• Anti-inflammatory effect of exercise training in subjects with type 2 diabetes and the metabolic syndrome is dependent on exercise modalities and independent of weight loss. (2010, background): “Recently, CRP, known to be produced primarily by the liver in response to inflammatory cytokines such as IL-6, was also shown to be generated in adipose tissue [9] and atherosclerotic plaques [10] and to actively participate in the pathogenesis of atherosclerosis by promoting endothelial cell activa”