Spatiotemporal correlation between HIF-1α and bone regeneration

Hypoxia-inducible factors (HIFs) are core regulators of the hypoxia response. HIF signaling is activated in the local physiological and pathological hypoxic environment, acting on downstream target genes to synthesize the corresponding proteins and regulate the hypoxic stress response. HIFs belong to the hypoxia-activated transcription family and contain two heterodimeric transcription factors, HIF-alpha and HIF-beta. Under hypoxia, the dimer formed by HIF-alpha binding to HIF-beta translocates into the nucleus and binds to the hypoxia response element (HRE) to induce transcription of a series of genes. HIF-1 alpha plays an important role in innate bone development and acquired bone regeneration. HIF-1 alpha promotes bone regeneration mainly through the following two pathways: (1) By regulating angiogenesis-osteoblast coupling to promote bone regeneration; and (2) by inducing metabolic reprogramming in osteoblasts, promoting cellular anaerobic glycolysis, ensuring the energy supply of osteoblasts under hypoxic conditions, and further promoting bone regeneration and repair. This article reviews recent basic research on HIF-1 alpha and its role in promoting osteogenesis, discusses the possible molecular mechanisms, introduces the hypoxia-independent role of HIF-1 alpha and reviews the application prospects of HIF-1 alpha in tissue engineering.

Automated summary

This article reviews the role of HIF-1 alpha in promoting osteogenesis, discusses its possible molecular mechanisms, and introduces its application prospects in tissue engineering.