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Abstract
Psoriasis is a multifactorial skin disorder with known systemic consequences. While most recent studies point to a predominantly Th17-driven process, psoriasis also lies at the crossroads linking the pathways of angiogenesis and inflammation. Mediators such as VEGF and angiopoietin-2 play significant roles in the pathophysiology and may even account for the maintenance of the chronic inflammatory state. Targets in this shared pathway may offer alternative avenues for therapy.