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The collateral vessel network consists of blood vessels that naturally form anatomical connections (“anastomoses”) between adjacent arterial trees, allowing for alternate routes of blood flow if a primary vessel is blocked[1][2][3][5][7]. These vessels may be present from embryonic development (via processes such as collaterogenesis), or they may adaptively remodel and expand (arteriogenesis) in response to local ischemia or vessel occlusion[1][2][6]. Their physiological role is critical in protection against tissue death due to vascular obstruction in the heart (coronary arteries), brain (circle of Willis, leptomeningeal collaterals), and peripheral tissues. The collateral vessel network is not an individual molecule, protein, or receptor and thus is not a direct therapeutic target; however, modulating its formation and maintenance (e.g., via growth factors or mechanical/inflammatory signals) is an area of research for the treatment of cardiovascular and cerebrovascular diseases[1][2][3][4][5][6][7].
Not applicable for drugs specifically targeting this network, but: VEGF pathway activation promotes collateral vessel growth (“collaterogenesis”); Notch pathway modulation affects endothelial cell sprouting during vessel formation; Inflammatory cytokines and monocyte recruitment facilitate remodeling (“arteriogenesis”).
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