Toll like receptor 4 in atherosclerosis and plaque destabilization.
The immune system plays a pivotal role in initiation and progression of atherosclerosis. Monocytes and T-lymphocytes are the first cells to enter the damaged endothelium. Differentiation of monocytes into macrophages and ingestion of lipids by these macrophages turning them into foam cells is a crucial step in the development of a fatty streak, the first sign of atherosclerosis. In recent years there has been accumulating evidence for the involvement of Toll like receptor 4, a pattern recognition receptor of the innate immune system, in the pathogenesis of atherosclerosis. Different cell types present in the atherosclerotic plaque express TLR4 and several pro-atherogenic ligands have been shown to activate TLR4. The innate immune system and the TLR signaling cascade may play an important role not only in the pathogenesis of atherosclerosis, but also in plaque destabilization. In this review, we discuss the role of TLR4 in the pathogenesis of atherosclerosis and vulnerable plaque development.
den Dekker
Wijnand K
WK
Molecular Cardiology Laboratory, Experimental Cardiology, Thoraxcenter, Erasmus Medical Center, Rotterdam, The Netherlands.
Cheng
Caroline
C
Pasterkamp
Gerard
G
Duckers
Hencricus J
HJ
D000818:Animals; D050197:Atherosclerosis / Q000209:etiology / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007113:Immunity, Innate / Q000502:physiology*; D053594:Myeloid Differentiation Factor 88 / Q000502:physiology; D011110:Polymorphism, Genetic; D015398:Signal Transduction; D051197:Toll-Like Receptor 4 / Q000235:genetics / Q000502:physiology*
D053594:Myeloid Differentiation Factor 88; D051197:Toll-Like Receptor 4