Expression of angiotensin II and interleukin 6 in human coronary atherosclerotic plaques: potential implications for inflammation and plaque instability.

By B. Schieffer, Elisabeth Schieffer, D. Hilfiker-Kleiner, A. Hilfiker, P. Kovanen, M. Kaartinen, J. Nussberger, W. Harringer, Helmut Drexler. Circulation, 2000

715 citations recorded by the source corpus.

Subfields: Cardiology and Cardiovascular Medicine, Immunology

View Paper: https://www.semanticscholar.org/paper/5e28b110c99eae45b78ed48bd21e150e85f8cfec

How researchers see this paper

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

In Cardiology and Cardiovascular Medicine

1. Thomas Braun
2. K. Griendling
3. P. Mehta
4. S. Dikalov

In Immunology

1. P. Mehta
2. V. Bronte
3. K. Griendling
4. M. Pittet
5. D. Gabrilovich
6. Rhian M. Touyz
7. E. Schiffrin
8. S. Dikalov

Citations in the corpus

• Angiotensin II cell signaling: physiological and pathological effects in the cardiovascular system. (2007, background): “In monocytes, macrophages, VSMCs, and endothelial cells, ANG II activates NF- B, which induces the production of cell adhesion molecules such as VCAM-1, ICAM-1, and E-selectin, and chemokines such as monocyte chemoattractant protein (MCP-1), IL-6, and IL-8 (157, 158, 167).”
• Acquisition of the contractile phenotype by murine arterial smooth muscle cells depends on the Mir143/145 gene cluster. (2009, background): “Vascular lesions result in activation of angiotensin II signaling, which together with other factors favors the acquisition of a synthetic phenotype (31).”
• The spleen in local and systemic regulation of immunity (2013, background): “Myocardial infarction and atherosclerosis in humans are also associated with increased AngII activity (McAlpine andCobbe, 1988; Schieffer et al., 2000); thus blocking AngII signaling could restrain the amplification of deleterious macrophages in these diseases as well.”