Figure 1.

Triggering receptors expressed on myeloid cells-1 (TREM-1) in the pathogenesis of atherosclerosis leading to acute myocardial infarction. (a) oxidized low density lipoprotein (oxLDL) concentration elevation in the plasma induces TREM-1 upregulation and its ligand interaction, leading to downstream signaling. TREM-1 interacts with DAP-12 to induce proinflammatory cytokines, chemokines, and cell surface molecule transcription through PI3K and PLC-α and nuclear factors NFAT and NF-κB. (b) The chronic inflammation condition induces the proliferation, recruitment, and differentiation of monocytes to macrophages which, in turn, uptake the oxLDL to form foam cells. It also induces the proliferation of smooth muscle cells (SMCs) that play a similar role. Altogether they form the atheroma. (c) The destabilization of the atheroma plaque causes coronary artery clog, resulting in acute myocardial infarction (AMI). During AMI, TREM-1 upregulation also induces a deleterious cardiac wall scar, which is a source of heart failure.