Arteriogenesis Versus Angiogenesis: Two Mechanisms of Vessel Growth (original) (raw)
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Arterial regeneration by collateral artery growth (arteriogenesis)
Drug Discovery Today: Disease Models, 2004
After birth, blood vessel growth is limited to two major processes. The growth of new capillaries by sprouting or INTUSSUSCEPTION (see Glossary) after the emergence of ischemia is called angiogenesis. By contrast, arteriogenesis describes the formation of collateral arteries from a pre-existing arteriolar network after the occlusion of a major artery. Physical forces, particularly fluid shear stress, induced by the increased blood velocity owing to low distal pressure, are triggers of arteriogenesis.
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Angiogenesis is the physiologic formation of new vessels from existent vascular bed. Angiogenic branching is regulated by balance of angiogenic activators and angiogenic inhibitors. The most remarkable factor affecting angiogenesis is vascular endothelial growth factor which acts via receptor tyrosin kinase. Ongoing studies on angiogenesis also highlight therapeutic approaches for tumor metastasis and metabolic diseases.
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Arteriosclerosis, Thrombosis, and Vascular Biology, 2003
Growth of collateral vessels is potentially able to preserve structure and a variable degree of function in subtended tissues in the presence of arterial occlusions. The process of transformation of a small arteriole into much larger conductance artery is called arteriogenesis. Small arterioles that interconnect side branches proximal from the arterial occlusion with distal ones experience increased fluid shear stress because of the increased blood flow velocity attributable to the pressure gradient along the bridging collaterals. This activates the endothelium and leads to monocyte adhesion and infiltration with the subsequent production of growth factors and proteases. Preexistent arterioles are essential. Their presence is genetically determined. Arteriogenesis is not organ-or species-specific; coronary or peripheral collateral vessels develop following the same design principles in mice, rats, rabbits, or dogs. In contrast to angiogenesis, arteriogenesis is not dependent on the presence of hypoxia/ischemia. (Arterioscler Thromb Vasc Biol. 2003;23:1143-1151.)
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Microcirculation, 2003
In patients with atherosclerotic vascular diseases, collateral vessels bypassing major arterial obstructions have frequently been observed. This may explain why some patients remain without symptoms or signs of ischemia. The term "arteriogenesis" was introduced to differentiate the formation of collateral arteries from angiogenesis, which mainly occurs in the ischemic, collateral flowdependent tissue. Many observations in various animal models and humans support that the remodeling of preexisting collateral vessels is the mechanism of collateral artery formation. This remodeling process seems to be mainly flowmediated. It involves endothelial cell activation, basal membrane degradation, leukocyte invasion, proliferation of vascular cells, neointima formation (in most species studied), and changes of the extracellular matrix. The contribution of ischemia to arteriogenesis is still unclear, but arteriogenesis clearly can occur in the absence of any significant ischemia. It is questionable, whether collateral arteries also form de novo in ischemic vascular diseases. A better understanding of the mechanisms of arteriogenesis will be important for the design of more effective strategies for the treatment of patients with ischemic vascular diseases. Microcirculation (2003) 10, 83-97. Arteriogenesis A Helisch and W Schaper 84 Arteriogenesis A Helisch and W Schaper 85 Arteriogenesis A Helisch and W Schaper 91 Arteriogenesis A Helisch and W Schaper 93 Arteriogenesis A Helisch and W Schaper 94
Acta Biochimica et Biophysica Sinica, 2008
Patients with occlusive atherosclerotic vascular diseases have frequently developed collateral blood vessels that bypass areas of arterial obstructions. The growth of these collateral arteries has been termed "arteriogenesis", which describes the process of a small arteriole's transformation into a much larger conductance artery. In recent years, intensive investigations using various animal models have been performed to unravel the molecular mechanisms of arteriogenesis. The increasing evidence suggests that arteriogenesis seems to be triggered mainly by fluid shear stress, which is induced by the altered blood flow conditions after an arterial occlusion. Arteriogenesis involves endothelial cell activation, basal membrane degradation, leukocyte invasion, proliferation of vascular cells, neointima formation (in most species studied), changes of the extracellular matrix and cytokine participation. This paper is an in-depth review of the research critical to recent advances in the field of arteriogenesis that have provided a better understanding of its mechanisms.
Vascular Embryology and Angiogenesis
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In simple terms, the cardiovascular system consists of a sophisticated pump (i.e., the heart) and a remarkable array of tubes (i.e., the blood and lymphatic vessels). Arteries and arterioles (the efferent blood vessels in relation to the heart) deliver oxygen, nutrients, paracrine hormones, blood and immune cells, and many other products to the capillaries, small-caliber, thin-walled vascular tubes. These substances are then transported through the capillary wall into the extravascular tissues, where they participate in critical physiological processes. In turn, waste products are transported from the extravascular space back into the blood capillaries and returned by the venules and veins (the afferent vessels) to the heart. Alternatively, approximately 10% of the fluid returned to the heart courses via the lymphatic system to the large veins. To develop normally, the embryo requires the delivery of nutrients and removal of waste products beginning early in development, and, indeed...