Inflammatory Mediators in Vascular Disease: Identifying Promising Targets for Intracranial Aneurysm Research

Figure 1

Summary of known and hypothesized contributions of macrophages and dendritic cells to intracranial aneurysm (IA). Interactions that have been demonstrated in IA models are depicted with solid arrows. Additional mechanisms that may be hypothesized based on other vascular inflammatory diseases are depicted with dotted arrows. Hemodynamic shear stress contributes to the recruitment of macrophages to the aneurysm wall via expression of MCP-1, a process that may also be aided by cell adhesion molecules. Macrophages are likely activated by IFN-γ and have been shown to contribute to IA by the secretion of TNF-α and MMPs. Additionally, macrophages and dendritic cells could contribute to inflammation via the presentation of DAMPs (such as oxidized lipids) on MHCII.