Development on the interaction between hypoxia inducible factor-1α and nuclear factor-κB in inflammatory hypoxic environment

Chronic inflammation is the pathological basis of a series of refractory diseases, such as cardiovascular injury, inflammatory bowel disease and cancer. Hypoxia is an important pathophysiological mechanism of tissue damage caused by chronic inflammation. Hypoxia inducible factor-1α (HIF-1α) can regulate tissue adaptation to hypoxia. During hypoxia, HIF-1α coordinates oxygen supply and metabolic activity in hypoxic tissues by activating adaptive transcriptional responses, which involve the up-regulation of cytokines such as angiogenic factors and vasoactive substances. Nuclear factor-κB (NF-κB), the key factor regulating immune response and apoptosis, has a similar function to HIF-1α, i. e., regulating hypoxia by changing the activity of oxygen-dependent proline hydroxylase under hypoxic conditions. This review discusses the interaction between HIF-1α and NF-κB activation pathways in a variety of chronic inflammatory diseases and the potential of both HIF-1α and NF-κB activation pathways as therapeutic targets for inflammatory diseases. Key words: Inflammation; Anoxia; Hypoxia-inducible factor 1, alpha subunit; NF-kappa B