A number of infectious agents have been associated with atherosclerotic cardiovascular disorders, including Chlamydia pneumoniae , Helicobacter pylori , cytomegalovirus (CMV) , Epstein-Barr virus , human immunodeficiency virus , herpes simplex viruses (HSV)1 , HSV2 , and hepatitis B  and C . More recent models emphasize the relationship of atherosclerosis to total "infectious burden" rather than specific pathogens . The above mentioned infectious agents or derived PAMPs have been shown to signal through one or more TLRs (Fig. 2). Furthermore, the recently identified cytoplasmatic PRR NOD1 (nucleotide-binding oligomerization domain) has been proposed to be involved in Chlamydia and Helicobacter induced signal transduction [57, 58]. It is intriguing to
TLR signaling pathway and its relevance to atherogenesis
Endogenous and exogenous molecules associated with lesion formation are thought to signal through TLR4 but the potential role of other TLRs has not yet been investigated. Interaction between ligand and receptor leads to the activation of NF-kB- or IRF3-responsive genes associated with progression of or protection against atherosclerosis. Endogenous or exogenous ligands can stimulate TLR-bearing cells, such as macrophages, dendritic cells (DCs), endothelial cells (EC), and smooth muscle cells (SMC). Minimally modified LDL (MM-LDL) can stimulate EC and SMC secretion of proinflammatory cytokines and chemokines, and also upregulates expression of adhesion molecules. Secreted chemokines attract monocytes to the endothelium, where these EC adhesion molecules facilitate leukocyte retention and subsequent migration into the subendothelial space, where they differentiate into macrophages under the influence of proinflammatory cytokines and growth factors. Uptake of modified LDL by macrophages via scavenger receptors initially protects ECs and SMCs from stimulation by modified LDL. However, persistent hypercholesterolemia leads to excessive cellular uptake of modified LDL, intracellular accumulation of cholesteryl esters, formation of foam cell, and eventually apoptosis and release of proinflammatory oxidized lipid derivatives into the plaque, further exacerbating the inflammatory nidus.
speculate if NODs are also involved in or associated with the development of atherosclerosis.
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