A major role for VCAM-1, but not ICAM-1, in early atherosclerosis.

By M. Cybulsky, K. Iiyama, Hongmei Li, Su-Ning Zhu, Mian Chen, M. Iiyama, V. Davis, J. Gutiérrez-Ramos, P. Connelly, D. Milstone. Journal of Clinical Investigation, 2001

1,238 citations recorded by the source corpus.

Subfields: Immunology, Immunology and Allergy, Radiology, Nuclear Medicine and Imaging

View Paper: https://www.semanticscholar.org/paper/a1f5b682b0285e49b08e1c12367233673709cfab

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In Immunology

1. Peter Libby
2. G. Hansson
3. K. Woollard
4. A. Tall
5. Karin E. Bornfeldt
6. F. Geissmann
7. Shu Chien
8. J. Chiu

In Immunology and Allergy

1. María Yáñez-Mó
2. Peter Libby

In Radiology, Nuclear Medicine and Imaging

1. Peter Libby

Citations in the corpus

• The immune response in atherosclerosis: a double-edged sword (2006, background): “Similarly, Ldlr −/− mice that express a truncated form of VCAM1 with impaired function develop less severe disease than those expressing wild-type VCAM1 (Ref”
• Adhesion molecules and atherosclerosis. (2003, background): “[145] Cybulsky MI, Iiyama K, Li H, Zhu S, Chen M, Iiyama M, et al.”
• A Critical Role of Platelet Adhesion in the Initiation of Atherosclerotic Lesion Formation (2002, background): “Both VCAM-1 and MCP-1 initiate monocyte recruitment and subsequent transmigration across the endothelial monolayer into the intima (12, 34) and have been shown to play a central role in atherosclerotic lesion formation (22, 23).”
• Role of oxidative modifications in atherosclerosis. (2004, background): “Early atherosclerotic events and the initiation of lesion formation appear particularly dependent on vascular cell adhesion molecule-1 (173).”
• Inflammation and cardiovascular disease mechanisms. (2006, background): “Despite similar cholesterol concentrations, lipoprotein profiles, and circulating leukocyte concentrations, mice prone to atherosclerosis because they cannot produce LDL receptororapolipoprotein(apo)Ebutengineeredtoexpressonly apoorlyfunctioningformofVCAM-1showasignificantreduction in lesion formati”
• Effects of Disturbed Flow on Vascular Endothelium: Pathophysiological Basis and Clinical Perspectives (2011, background): “Despite these differences, the pathological inflammatory responses of the two cell types involve similar mediators such as ICAM-1, VCAM-1, and E-selectin (398).”
• Dynamic interaction of VCAM-1 and ICAM-1 with moesin and ezrin in a novel endothelial docking structure for adherent leukocytes (2002, background): “In addition, VCAM-1 may play an im- 1240 The Journal of Cell Biology | Volume 157, Number 7, 2002 portant role in the pathogenesis of diseases such as atherosclerosis (Cybulsky et al., 2001), rheumatoid arthritis (Carter and Wicks, 2001), and multiple sclerosis (Alon, 2001).”
• Inflammation in atherosclerosis (2002, background): “However, experiments with hypomorphic variants of VCAM-1 introduced into mice rendered susceptible to atherogenesis (by inactivation of the apolipoprotein E ( apoE ) gene) show reduced lesion formatio”
• Endothelial Cell Dysfunction and the Pathobiology of Atherosclerosis (2016, positive): “Finally, its genetic deficiency in mouse models of atherosclerosis results in a reduction in lesion formation.(108) These findings thus highlighted the pathogenic significance of VCAM-1 in the context of atherogenesis, and also implicated it as a molecular marker of ECD in the clinical setting.”