Arteriogenesis

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The term arteriogenesis describes the development of a natural bypass after a vascular occlusion ( stenosis ), for example in the heart or in the leg (peripheral occlusion) in humans, but also in the experimental animal model. In the process, very small blood vessels ( arterioles ) grow (proliferate) into much larger blood vessels ( arteries ).

Mechanism of arteriogenesis

The process is made possible by dilation of the vascular lumen, the accumulation of myocytes ( smooth muscle cells ) and hypertrophy of the vascular endothelium. The trigger for arteriogenesis is a stenosis of a supplying blood vessel. The lowered perfusion pressure, but above all shear forces ( shear stress ) in the remaining blood vessels causes an activation of the endothelium. The latter in turn leads to an inflammatory reaction with the release of nitric oxide and transcription factors such as HIF-1α (hypoxia-induced factor) and ultimately to the release of cytokines such as MCP-1 (monocyte chemotactic protein-1). Furthermore, an activation of inflammatory cells - mainly monocytes and macrophages - and an increased gene expression of adhesion molecules ( intracellular adhesion molecule-1 , ICAM-1) are induced.

In arteriogenesis, the vessel diameter can be increased by 20 times the initial diameter. In most cases, this enables an adequate blood supply again.

Medical research attempts to stimulate arteriogenesis with certain substances, such as granulocyte-macrophage colony-stimulating factor (GM-CSF). This means that new therapies for the treatment of cardiovascular diseases should be available in the future .

Differentiation from angiogenesis

In contrast to angiogenesis , arteriogenesis takes place independently of an oxygen supply ( hypoxia ).

Individual evidence

  1. ↑ Schaper W, Buschmann I, Arteriogenesis, the good and bad of it. In: Cardiovasc Res , 43/1999, pp. 835-7.
  2. ↑ Scholz D et al., Arteriogenesis, a new concept of vascular adaptation in occlusive disease. In: Angiogenesis , 4/2001, pp. 247-57.
  3. ↑ a b c Armbruster WH, Transgenic Revascularization by Growth Factors on the Porcine Chronic Ischemic Myocardium - Evaluation of Regional Contractility , Dissertation, Albert-Ludwigs-Universität Freiburg, 2006
  4. ^ Pipp F et al., Elevated fluid shear stress enhances postocclusive collateral artery growth and gene expression in the pig hind limb. In: Arterioscler.Thromb.Vasc.Biol. , 24/2004, pp. 1664-8.
  5. ^ Price RJ et al., Hemodynamic stresses and structural remodeling of anastomosing arteriolar networks; design principles of collateral arterioles. In: Microcirculation , 9/2002, pp. 111-24.
  6. ↑ Schaper W, Scholz D, Factors regulating arteriogenesis. In: Arterioscler.Thromb.Vasc.Biol. , 23/2003, pp. 1143-51.

literature

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