缺氧诱导因子-1α在溃疡性结肠炎发病机制中的研究进展

Research progress on hypoxia-inducible factor-1α in pathogenesis of ulcerative colitis

溃疡性结肠炎(ulcerative colitis,UC)是一种结直肠慢性非特异性炎症性疾病,发病机制尚未完全明确。缺氧诱导因子(hypoxia-inducible factor,HIF)-1α直接或间接参与UC发生机制,引起肠道菌群失调,导致肠腔内致病菌和条件致病菌增多,同时肠黏膜屏障结构被破坏,使血管通透性增加,肠腔内细菌及细菌产物向黏膜固有层移位,引起免疫细胞的激活及炎症细胞浸润,进而血清中促血管生成因子水平升高,与血管生成抑制因子的作用失衡,导致病理性血管生成,从而诱发UC的进展。该文主要汇总HIF-1α在UC进程中的作用机制,为该因子对溃疡性结肠炎的治疗及药物研发提供创新思路。

Ulcerative colitis(UC)is a chronic nonspecific inflammatory disease of the colorectal,and its pathogenesis has not been fully defined.Hypoxia-inducible factor(HIIF)-1αis directly or indirectly involved in the pathogenesis of UC,causing intestinal flora imbalance,resulting in the increase of enterogenic and conditioned pathogens,and the destruction of intestinal mucosal barrier structure,resulting in increased vascular permeability.Intestinal bacteria and bacterial products migrate to mucosal laminae propria,causing activation of immune cells and infiltration of inflammatory cells,thus increasing the level of serum pro-angiogenesis factors and imbalance of the effect of angiogenesis inhibitors,leading to pathological angiogenesis,thus inducing the progression of UC.This paper mainly summarized the mechanism of HIF-1αin the UC process,and provides innovative ideas for the treatment of ulcerative colitis by this factor and drug development.