Figure 7.
An illustration of potential mechanisms in injury-induced vascular intimal hyperplasia is depicted. We propose that intimal hyperplasia is driven by toll-like receptor 4 (TLR4)–myeloid differentiation factor 2 (MD2) on macrophages responding to high-mobility group box 1 (HMGB1) released by injured and stressed cells in the vessel wall. Blockade of HMGB1–MD2 interaction could be a therapeutic target. For detailed discussion of the pathways, please see the text. DAMP indicates damage-associated molecular pattern molecule; and SMC, smooth muscle cell.