Background: A hallmark of atherosclerosis is its complex pathogenesis, which is dependent on altered
cholesterol metabolism and inflammation. Both arms of pathogenesis involve myeloid cells. Monocytes migrating
into the arterial walls interact with modified low-density lipoprotein (LDL) particles, accumulate cholesterol and
convert into foam cells, which promote plaque formation and also contribute to inflammation by producing proinflammatory
cytokines. A number of studies characterized transcriptomics of macrophages following interaction
with modified LDL, and revealed alteration of the expression of genes responsible for inflammatory response and
cholesterol metabolism. However, it is still unclear how these two processes are related to each other to contribute
to atherosclerotic lesion formation.
Methods: We attempted to identify the main mater regulator genes in macrophages treated with atherogenic
modified LDL using a bioinformatics approach.
Results: We found that most of the identified genes were involved in inflammation, and none of them was
implicated in cholesterol metabolism. Among the key identified genes were interleukin (IL)-7, IL-7 receptor, IL-
15 and CXCL8.
Conclusion: Our results indicate that activation of the inflammatory pathway is the primary response of the
immune cells to modified LDL, while the lipid metabolism genes may be a secondary response triggered by