FIGURE 9.

Schematic illustration describing the underlying mechanism of insulin‐like growth factor‐binding protein 5 (IGFBP5)‐regulated endothelial cell angiogenesis post‐hindlimb ischaemia (HLI). After HLI, IGFBP5 production was promoted, which inhibited the action of IGF1/2 and the phosphorylation of IGF1R and ATP production, thereby promoting the ubiquitin‐ligase Von Hippel‐Lindau (VHL) and the ubiquitination and degradation of HIF1α. When deficiency of IGFBP5 in endothelial cells (ECs), the IGF1R phosphorylation was promoted, the ATP production was promoted, and the ubiquitination of HIF1α was suppressed, which promoted angiogenesis post‐HLI.