缺氧在银屑病发病机制中的作用  

Roles of hypoxia in the pathogenesis of psoriasis

作　　者：王焕玲[1] 魏志平[1] 刘彦群[1] 

机构地区：[1]徐州医学院附属医院皮肤科,江苏221002

出　　处：《国际皮肤性病学杂志》2016年第3期164-167,共4页International Journal of Dermatology and Venereology

摘　　要：银屑病是一种以鳞屑性红斑、丘疹、斑块为主要临床表现的皮肤病,其表皮角质形成细胞的过度增殖使其具备类似肿瘤的生物学行为,与肿瘤组织一样,均存在局部缺氧现象.缺氧可使角质形成细胞低氧诱导因子1 α及其相关的多种基因,如血管内皮生长因子、一氧化氮合酶、基质金属蛋白酶2、环氧合酶2、胰岛素样生长因子2、神经生长因子、组蛋白去乙酰化酶1和LL37等因子的表达升高,从而促进炎症细胞浸润、表皮细胞增生和血管形成.缺氧还可使角质形成细胞糖酵解有关酶的表达增高,使得细胞糖酵解功能增强,从而满足细胞快速增殖的能量需求.Psoriasis is a kind of skin disease mainly characterized by squamous erythema,papules and plaques.Like tumor tissue,psoriatic lesions show keratinocyte overproliferation and regional hypoxia.Hypoxia can promote the infiltration of inflammatory cells,proliferation of epidermal cells and vascularization by increasing expressions of hypoxia-inducible factor 1α （HIF-1o） and its related genes,such as vascular endothelial growth factor （VEGF）,nitric oxide synthase （NOS）,matrix metalloproteinase-2 （MMP-2）,cyclooxygenase 2 （COX-2）,insulin-like growth factor 2 （IGF2）,nerve growth factor （NGF）,histone deacetylase 1 （HDAC1）,cathelicidin LL37,and so on.Hypoxia also can enhance glycolysis via upregulating expressions of relevant enzymes in keratinocytes,so as to meet energy requirements of rapid cell proliferation.

关 键 词：银屑病 缺氧 HIF-1 α 一氧化氮 靶基因 

分 类 号：R758.63[医药卫生—皮肤病学与性病学]