Summary
Angiogenesis is a hallmark of
chronic inflammation such as psoriasis. Unraveling the pathogenesis
of psoriasis shows that several proangiogenic mediators are
activated and highly expressed during psoriasis. Vascular
endothelial growth factor, hypoxia- inducible factor, tumor
necrosis factor, interleukin-8 and angiopoietins are considered to
be the main players responsible for the strong vessel formation in
psoriasis. The proangiogenic milieu in the skin seems to result
from a proinflammatory immune response initiated by T helper cells.
Interestingly, several small molecules as well as modern biologics
used for systemic therapy of psoriasis have been shown to provide
not only immune regulatory effects but also influence endothelial
cell biology. Thus, direct targeting of angiogenesis may not only
help to understand psoriasis pathogenesis but also to develop new
strategies to treat psoriasis with therapeutics that halt the
angiogenesis required for the inflammatory disease.