Inflammatory bowel disease (IBD) develops as a result of a combination of genetic predisposition, dysbiosis of the gut microbiota, and environmental influences, which is mainly represented by ulcerative colitis (UC) and Crohn's disease (CD). IBDs can result in inflammatory hypoxia by causing intestinal inflammation and vascular damage. The hypoxia-inducible factor 1-alpha (HIF-1α), as a transcription factor, can regulate the cellular adaptation to low oxygen levels and support the development and function of the gut barrier. HIF-αplays its functions through translocating into the nucleus, dimerizing with HIF-1β, and binding to hypoxia-responsive elements of HIF-1 target genes. So far, most studies have addressed the function of HIF-1α in murine models of IBD. In this review, we aim to outline the major roles of HIF-1α in the IBD.
Keywords: hypoxia-inducible factor-1 α (HIF-1α); immune cell; inflammatory bowel disease (IBD); intestinal epithelial cell (IEC).
© 2021 International Federation for Cell Biology.