Atherosclerotic Plaque Progression and Vulnerability to Rupture: Angiogenesis as a Source of Intraplaque Hemorrhage

By Renu Virmani, F. Kolodgie, A. Burke, A. Finn, H. Gold, T. Tulenko, S. Wrenn, J. Narula. Arteriosclerosis, Thrombosis and Vascular Biology, 2005

1,406 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology, Surgery

View Paper: https://www.semanticscholar.org/paper/b03d106cba56a2381261b28a600bcfb02b85571d

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. Erling Falk
2. J. Bentzon
3. Renu Virmani
4. G. Owens
5. F. Otsuka
6. A. Poole
7. Ewelina Gołębiewska

In Molecular Biology

1. Gautam Sethi
2. Delphine Gomez
3. G. Owens

In Surgery

1. Erling Falk
2. J. Bentzon
3. F. Otsuka
4. Renu Virmani

Citations in the corpus

• Smooth muscle cell phenotypic switching in atherosclerosis. (2012, background): “Evidence of SMC transition into alternative states raises major questions related to the potential participation of SMC in several aspects of human atherogenesis and atherosclerotic lesion progression, including fibrous cap formation but also neovascularization and haemorrhagic events within the adv”
• The Vascular Endothelium and Human Diseases (2013, background): “Furthermore, thrombus reorganization following subacute rupture has been proposed as a mechanism for lesion progression (37-39).”
• Research Progress on the Relationship between Atherosclerosis and Inflammation (2018, background): “Studies have found that VCAM-1 and ICAM-1 were closely related to angiogenesis [34].”
• Mechanisms of plaque formation and rupture. (2014, background): “Other Associated Features of Plaque Rupture Additional plaque features are more common in ruptured plaques than in intact plaques, including increased neovascularization and adventitial inflammation.(140,141) Furthermore, culprit lesions for ACS are generally less calcified than plaques responsible ”
• Platelets in Inflammation and Atherogenesis (2015, background): “These mechanisms ultimately result in plaque destabilization (132).”