Vascular proliferation and angiogenic factors in psoriasis

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Abstract
Psoriasis is a common, chronic skin disorder characterized by hyperproliferation of the epidermis, inflammatory cell accumulation and increased tortuosity and dilatation of dermal papillary blood vessels. Research into the pathogenesis of psoriasis has concentrated mainly on the interplay between inflammatory cells and epidermal proliferation. Central to the proposed pathogenetic pathway are cytokines produced by activated keratinocytes, which are thought to induce both keratinocyte proliferation and lymphocyte migration. Cytokines also mediate upregulation of adhesion molecules on vascular endothelium which in turn permits lymphocyte recruitment. The close spatial relationship between altered microvasculature and epidermis is clearly important in psoriasis. Consequently, understanding the mechanisms underlying vascular changes is fundamental to an elucidation of pathogenetic mechanisms in psoriasis.