Department of Dermatology, University of California, Davis, Sacramento, CA 95816, USA.
J Dermatol Sci. 2011 Jul;63(1):1-9. doi: 10.1016/j.jdermsci.2011.04.007. Epub 2011 Apr 27.
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.
银屑病和动脉粥样硬化的病理生理学基础存在血管生成和氧化的共同机制。在这两种疾病的发病机制中，损伤或局部缺氧等刺激会引发包括白细胞介素-8（IL-8）、缺氧诱导因子-1α（HIF-1α）、ETS-1 和血管内皮生长因子（VEGF）等促血管生成因子的释放。这些因子通过增强细胞黏附分子的表达，刺激通透性增加，并促使白细胞迁移到炎症部位。银屑病和动脉粥样硬化也有共同的活性氧（ROS）酶源，这些 ROS 影响几种细胞信号通路，这些信号通路与这两种疾病的发病机制有关。针对这些通路中的关键因素的药物和基因治疗方法，可能为银屑病的治疗提供创新方法，并可能减轻银屑病患者的心血管并发症。
