Inhibition of plaque neovascularization reduces macrophage accumulation and progression of advanced atherosclerosis

By K. Moulton, K. Vakili, D. Zurakowski, Mohsin Q. Soliman, C. Butterfield, E. Sylvin, K. Lo, S. Gillies, K. Javaherian, J. Folkman. Proceedings of the National Academy of Sciences of the United States of America, 2003

700 citations recorded by the source corpus.

Subfields: Immunology, Immunology and Allergy, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/82c000d66a80c8c81b76c493b4ef41413cde3f9b

How researchers see this paper

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

In Immunology

1. K. Woollard
2. M. C. Simon
3. F. Geissmann

In Molecular Biology

1. M. C. Simon
2. J. Folkman
3. Bryan L. Krock
4. K. Woollard
5. Nicolas Skuli
6. F. Geissmann
7. Nicola Bellomo
8. G. Semenza

Citations in the corpus

• Monocytes in atherosclerosis: subsets and functions (2010, background): “This neovascularization can further contribute to cellular trafficking and recruitment through the vaso vasorum”
• Hypoxia-induced angiogenesis: good and evil. (2011, background): “Plaque perfusion promotes expansion by allowing more efficient infiltration of macrophages through new capillaries.(119) Interestingly, HIF-1α and VEGF are expressed in the plaque, suggesting that the HIF signaling pathway is directly involved in plaque angiogenesis.”
• Opinion: Angiogenesis: an organizing principle for drug discovery? (2007, background): “The concept of angiogenesis-dependent diseases originated in 1972 with the recognition that certain non-neoplastic diseases, such as the chronic inflammatory disease psoriasis, depend on chronic neovascularization to provide a conduit for the continual delivery of inflammatory cells to the inflammat”