Interferon-beta, a possible target in arteriogenesis.

Abstract

In patients with coronary or peripheral artery disease, restoration of perfusion can be achieved via the growth of collateral arteries, known as arteriogenesis. Circulating monocytes play a pivotal role as cellular modulators in the development of arteriogenesis. After monocyte adhesion to the endothelium of the collateral vessel, transmigrated monocytes secrete chemokines, proteases and growth factors. These secreted molecules are essential for arteriogenesis, through the induction and proliferation of smooth muscle cells (SMCs) and endothelial cells. In this thesis we consider body’s own cytokine interferon-beta (IFNβ) as a possible target in arteriogenesis, therefore it is interesting how to translate this statement into the field of research subsequently in a therapeutic treatment. Previously, in literature it has been described that IFNβ plays a pivotal role in the inhibition of arteriogenesis. This will be further discussed into detail by using comparable angiogenesis research performed in animal models. Finally, the discussion hypothesizes at least seven different IFNβ mediated mechanisms to promote arteriogenesis.