Table 2. Factors involved in AVM pathogenesis.
| Inflammatory mediators involved | Inflammatory pathway | |
|---|---|---|
| Leukocyte recruitment | IL-6, TNF-α, and IL-1β21 | Overexpression of E-selectin, ICAM-1, and VCAM-122 |
| Angiogenesis | IL-6, VEGF, HIF-1, NF-κB, IL-1β, and IL-821, 59, 64 | EC proliferation21, 22, 23, 43 EC migration22, 43 CAM expression22 Decreased EC apoptosis43 |
| Vascular instability | MIF, Caspase-3, MMP-9, IL-6, TNF-α, and VEGF23, 39, 40, 64 Decreased TIMP level30 | Macrophage recruitment39 ECM degradation40 Increased EC growth43 |
| Vascular permeability | VEGF68 | EC fenestrations ECM degradation65, 66, 67, 77 Sprouting angiogenesis69 |
| HCSMC proliferation | IL-623 | Upregulation of VEGF and MMP-923 |
CAM, cell adhesion molecule; EC, endothelial cell;90 ECM, extracellular matrix; HCSMC, human cerebral smooth muscle cell; HIF-1, hypoxia-inducible factor-1; ICAM-1, intercellular cell adhesion molecule-1; IL-6, interleukin-6; IL-1, interleukin-1; IL-8, interleukin-8; IL-1β, interleukin-1-beta; MIF, macrophage migration inhibitory factor; MMP, matrix metalloproteinase; NF-κB, nuclear factor-kappa B; TIMP, tissue inhibitor of metalloproteinase; TNF-α, tumor necrosis factor-alpha; VCAM-1, vascular cell adhesion molecule-1; VEGF, vascular endothelial growth factor.