More specifically, mechanical stresses cause endothelial cells to produce chemical facilitators that begin the process of increasing diameter.
This finding is important because it shows that arteriogenesis is the result of a combination of signaling cascades and growth factors as opposed to being tied to a single chemical.
Monocytes can enter the vessel wall to become macrophages and produce inflammatory cytokines such as TNF-α in addition to aiding the production of bFGF and MMP (Van Royen et al., 2000).
One study showed that local infusion of MCP-1 caused a large increase in conductance in both collateral and peripheral vessels while diminished levels of MCP-1 hindered the process of arteriogenesis (Ito et al., 1997).
Sprint training is a type of anaerobic exercise that relies on having the maximum amount of blood available to the vessel network at any given time (Prior et al., 2004).
Presently, the effects of arteriogenesis on atherosclerosis are unknown, although MCP-1 receptors are known to be associated with plaque formation (Van Royen et al., 2001).