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Update on lipids, inflammation and atherothrombosis.
Thromb Haemost. 2011 May; 105 Suppl 1:S34-42.TH

Abstract

Atherosclerosis is an inflammatory disease that involves the arterial wall and is characterised by the progressive accumulation of lipids in the vessel wall. The first step is the internalisation of lipids (LDL) in the intima with endothelial activation which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. These events increase LDL particles accumulation in the extracellular matrix where they aggregate/fuse, are retained by proteoglycans and become targets for oxidative and enzymatic modifications. In turn, retained pro-atherogenic LDLs enhance selective leukocyte recruitment and attachment to the endothelial layer inducing their transmigration across the endothelium into the intima. While smooth muscle cell numbers decline with the severity of plaque progression, monocytes differentiate into macrophages, a process associated with the upregulation of pattern recognition receptors including scavenger receptors and Toll-like receptors leading to foam cell formation. Foam cells release growth factors, cytokines, metalloproteinases and reactive oxygen species all of which perpetuate and amplify the vascular remodelling process. In addition, macrophages release tissue factor that, upon plaque rupture, contributes to thrombus formation. Smooth muscle cells exposed in eroded lesions are also able to internalise LDL through LRP-1 receptors acquiring a pro-thrombotic phenotype and releasing tissue factor. Platelets recognise ligands in the ruptured or eroded atherosclerotic plaque, initiate platelet activation and aggregation leading to thrombosis and to the clinical manifestation of the atherothrombotic disease. Additionally, platelets contribute to the local inflammatory response and may also participate in progenitor cell recruitment.

Authors+Show Affiliations

Cardiovascular Research Center, c/Sant Antoni Ma. Claret 167, Barcelona, Spain. lbadimon@csic-iccc.orgNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

21479344

Citation

Badimon, Lina, et al. "Update On Lipids, Inflammation and Atherothrombosis." Thrombosis and Haemostasis, vol. 105 Suppl 1, 2011, pp. S34-42.
Badimon L, Storey RF, Vilahur G. Update on lipids, inflammation and atherothrombosis. Thromb Haemost. 2011;105 Suppl 1:S34-42.
Badimon, L., Storey, R. F., & Vilahur, G. (2011). Update on lipids, inflammation and atherothrombosis. Thrombosis and Haemostasis, 105 Suppl 1, S34-42. https://doi.org/10.1160/THS10-11-0717
Badimon L, Storey RF, Vilahur G. Update On Lipids, Inflammation and Atherothrombosis. Thromb Haemost. 2011;105 Suppl 1:S34-42. PubMed PMID: 21479344.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Update on lipids, inflammation and atherothrombosis. AU - Badimon,Lina, AU - Storey,Robert F, AU - Vilahur,Gemma, Y1 - 2011/04/11/ PY - 2010/11/11/received PY - 2011/01/03/accepted PY - 2011/4/12/entrez PY - 2011/4/12/pubmed PY - 2011/7/30/medline SP - S34 EP - 42 JF - Thrombosis and haemostasis JO - Thromb. Haemost. VL - 105 Suppl 1 N2 - Atherosclerosis is an inflammatory disease that involves the arterial wall and is characterised by the progressive accumulation of lipids in the vessel wall. The first step is the internalisation of lipids (LDL) in the intima with endothelial activation which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. These events increase LDL particles accumulation in the extracellular matrix where they aggregate/fuse, are retained by proteoglycans and become targets for oxidative and enzymatic modifications. In turn, retained pro-atherogenic LDLs enhance selective leukocyte recruitment and attachment to the endothelial layer inducing their transmigration across the endothelium into the intima. While smooth muscle cell numbers decline with the severity of plaque progression, monocytes differentiate into macrophages, a process associated with the upregulation of pattern recognition receptors including scavenger receptors and Toll-like receptors leading to foam cell formation. Foam cells release growth factors, cytokines, metalloproteinases and reactive oxygen species all of which perpetuate and amplify the vascular remodelling process. In addition, macrophages release tissue factor that, upon plaque rupture, contributes to thrombus formation. Smooth muscle cells exposed in eroded lesions are also able to internalise LDL through LRP-1 receptors acquiring a pro-thrombotic phenotype and releasing tissue factor. Platelets recognise ligands in the ruptured or eroded atherosclerotic plaque, initiate platelet activation and aggregation leading to thrombosis and to the clinical manifestation of the atherothrombotic disease. Additionally, platelets contribute to the local inflammatory response and may also participate in progenitor cell recruitment. SN - 2567-689X UR - https://www.unboundmedicine.com/medline/citation/21479344/Update_on_lipids_inflammation_and_atherothrombosis_ L2 - http://www.thieme-connect.com/DOI/DOI?10.1160/THS10-11-0717 DB - PRIME DP - Unbound Medicine ER -