Author(s): Armstrong AW, Voyles SV, Armstrong EJ, Fuller EN, Rutledge JC
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Abstract Shared angiogenic and oxidative mechanisms underlie the pathophysiology of psoriasis and atherosclerosis. During the pathogenesis of both diseases, stimuli such as injury or local hypoxia trigger the release of pro-angiogenic factors including IL-8, HIF-1α, ETS-1, and VEGF. These factors stimulate increased permeability and encourage leukocyte transmigration into areas of inflammation by enhanced expression of cell adhesion molecules. Psoriasis and atherosclerosis also share common enzymatic sources of reactive oxygen species (ROS), and these ROS influence several cellular signaling pathways implicated in the pathogenesis of both diseases. Pharmacologic and genetic therapies that target key factors in these pathways could provide innovative approaches to the management of psoriasis and potentially mitigate the cardiovascular complications suffered by psoriasis patients. Copyright © 2011 Japanese Society for Investigative Dermatology. Published by Elsevier Ireland Ltd. All rights reserved.
This article was published in J Dermatol Sci
and referenced in Anatomy & Physiology: Current Research