Arteriogenesis

Arteriogenesis is the growth and remodeling of pre-existing arteries to form functional collateral vessels that bypass occluded or narrowed arteries. Unlike angiogenesis, which creates new capillaries from existing vessels, arteriogenesis enlarges and restructures existing arteriolar arches and major collateral arteries to accommodate increased blood flow.

The process is driven primarily by increased shear stress in collateral vessels following arterial occlusion or reduced distal perfusion. Endothelial cells sense shear stress and release signals that recruit inflammatory cells, particularly monocytes, which differentiate into macrophages in the vessel wall. This inflammatory milieu along with growth factors such as vascular endothelial growth factor and fibroblast growth factors, and remodeling enzymes like matrix metalloproteinases, promotes degradation and reorganization of the extracellular matrix, smooth muscle cell proliferation, and matrix deposition.

The result is the formation of larger, more muscular collateral arteries with improved conductance. Arteriogenesis occurs over days to weeks after the initiating event and requires intact vascular architecture and functional endothelium. The magnitude of arteriogenesis varies among individuals and is influenced by age, diabetes, hyperlipidemia, smoking, and other risk factors, which can impair monocyte recruitment and remodeling.

Clinical significance is its potential to mitigate ischemia in coronary, cerebral, and peripheral circulations. It is a target for therapies aiming to enhance collateral flow. Experimental approaches include interventions that augment shear stress responses, administration of cytokines or growth factors, cell therapy, and structured exercise to promote favorable hemodynamics.