Fig. 7

Redox signaling regulates the disease-related microenvironment. Under normoxic conditions, HIF-1α undergoes oxidative modifications, leading to its degradation through binding to VHL or sequestration in the cytoplasm via binding with p300. In hypoxic conditions, oxidative modifications decrease, allowing for nuclear translocation of HIF-1α and the transcriptional activation of genes related to angiogenesis, energy metabolism, cytokines, and matrix function. Activation of Toll-like receptors leads to the phosphorylation and degradation of IκB, releasing NF-κB complexes for nuclear transcription of genes associated with inflammatory factors. The p50 subunit can be modified by glutathionylation, hindering its binding to DNA. Inflammatory cytokines, TGF-β, HMGB, and other factors regulate the formation of the inflammatory microenvironment