摘要
婴幼儿血管瘤的发病机制尚不明确,缺氧理论成为目前的主要学说之一。该文综述了缺氧状态下血管瘤内皮细胞中缺氧诱导因子-1α及其靶基因的具体作用机制,HIF-1α表达增加,并激活其下游靶基因,如葡萄糖转运蛋白-1、血管内皮生长因子、B淋巴细胞瘤/白血病-2/腺病毒E1B 19000相互作用蛋白3、碳酸酐酶-Ⅸ、磷酸化的蛋白激酶B,从不同的病理生理角度(如糖代谢、血管生成、pH调节和细胞增殖等)使机体适应缺氧,促进了婴幼儿血管瘤的发生和发展。
The pathogenesis of infantile hemangioma is not clear,and hypoxia theory has become one of the main theories.Under hypoxia,cells activate numerous downstream target genes through the expression of hypoxia inducible factor-1α,such as glucose transporter-1,vascular endothelial growth factor,and B-cell lymphoma/Leukemia-2/adenovirus E1B 19000-interacting protein 3,carbonic anhydrase-Ⅸ,phosphorylated protein kinase B,from different pathophysiological perspectives(such as glucose metabolism,angiogenesis,pH regulation and cell proliferation,etc.)enable the body to adapt to hypoxia.This article reviews the specific mechanism of action of HIF-1αand its target genes,and provides a theoretical basis for how hypoxia plays a role in infantile hemangioma.
作者
金兰
丁媛
康晓静
Jin Lan;Ding Yuan;Kang Xiaojing(Xinjiang Medical University,Urumqi 830001,China;Department of Dermatology and Venereology,People′s Hospital of Xinjiang Uygur Autonomous Region,Urumqi 830001,China)
出处
《中华整形外科杂志》
CAS
CSCD
北大核心
2020年第4期453-456,共4页
Chinese Journal of Plastic Surgery
基金
自治区卫生计生委青年医学科技人才专项科研项目(WJWY201804)。
作者简介
通信作者:康晓静,Email:drkangxj666@163.com。