Molecular pathways used by platelets to initiate and accelerate atherogenesis.
OBJECTIVE
The response to injury model in the development of atherosclerosis is broadly accepted by the scientific audience. Platelets are generally not believed to be involved in the initiation of atherosclerosis. New data imply, however, that the response to injury model is too simple for a complete understanding of the inflammatory disease atherosclerosis. The involvement of platelets in the initiation of atherosclerotic lesion formation is critical in directing the atherosclerotic process into regeneration or ongoing vascular injury.


RESULTS
Platelets internalize oxidized phospholipids and promote foam cell formation. Platelets also recruit circulating blood cells including progenitor cells to the vessel, that are able to differentiate into foam cells or endothelial cells depending on conditions. Platelets express various scavenger receptors that are able to regulate LDL-uptake. LDL-laden platelets are internalized by adherent progenitor cells that in turn differentiate into macrophages and foam cells.


CONCLUSIONS
An expanding body of evidence continues to build on the role of platelets as initial actors in the development of atherosclerotic lesions. Platelets bind to leukocytes, endothelial cells, and circulating progenitor cells and initiate monocyte transformation into macrophages. Therefore platelets regulate the initiation, development and total extent of atherosclerotic lesions.
Lindemann
Stephan
S
Medical Clinic III, Cardiology and Circulatory Diseases, Eberhard Karls University, Tübingen, Germany.
Krämer
Björn
B
Daub
Karin
K
Stellos
Konstantinos
K
Gawaz
Meinrad
M
D000818:Animals; D050197:Atherosclerosis / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D001792:Blood Platelets / Q000378:metabolism* / Q000502:physiology; D004730:Endothelium, Vascular / Q000166:cytology / Q000378:metabolism; D005487:Foam Cells / Q000166:cytology / Q000378:metabolism; D006801:Humans; D008954:Models, Biological; D015398:Signal Transduction / Q000502:physiology