Arteriogenesis

Arteriogenesis is the physiological process of remodeling pre-existing collateral arterioles into larger, functional conductance arteries (Heil et al., 2006). Unlike angiogenesis, which is the sprouting of new capillaries driven by hypoxia, arteriogenesis is primarily driven by increased fluid shear stress following the occlusion of a major artery (Buschmann & Schaper, 1999). This process involves the activation of endothelial cells, the recruitment of inflammatory cells—particularly monocytes—and the subsequent proliferation of vascular smooth muscle cells to increase the vessel's lumen diameter (Schaper, 2009). In clinical contexts, arteriogenesis serves as a natural bypass to restore blood flow to ischemic tissues in conditions like coronary artery disease and peripheral artery disease (Simons, 2005). While therapeutic stimulation of arteriogenesis using growth factors like FGF-2 or GM-CSF has been investigated to treat obstructive vascular diseases, identifying specific molecular targets that can safely and effectively trigger this complex multicellular process remains a significant challenge in cardiovascular medicine (Seiler et al., 2001).

Other names

Collateral growthCollateral artery remodelingNatural bypass formationCollateralization

Therapeutic strategies aim to enhance arteriogenesis by increasing fluid shear stress, promoting the recruitment and adhesion of pro-inflammatory monocytes to the vessel wall, or directly stimulating the proliferation of endothelial and smooth muscle cells to expand collateral vessel diameter (van Royen et al., 2001).