Hypoxia-inducible factor-1α/β-catenin axis: A conserved regulatory hub for enhancing stem cell function in tissue regeneration

Table 1 Hypoxia-inducible factor-1α and β-catenin under different hypoxic contexts

Hypoxia model/biological context	Acute hypoxia (post-stroke recovery)	Chronic hypoxia (liver HBV replication)	Intermittent hypoxia (OSAS promotes cancer)
HIF-1α status	Significantly upregulated by delayed HBO via ROS induction	Stably highly expressed due to direct hypoxic stabilization	Markedly activated under IH conditions
β-catenin pathway status	Significantly activated (↑ protein expression & nuclear translocation)	Co-activated (↑ expression, functional synergy with HIF-1α)	Not truly activated (↑ mRNA, but no nuclear translocation)
Core regulatory mechanism	Forms a sequential ROS → HIF-1α → β-catenin signaling cascade	HIF-1α and β-catenin show spatial co-expression and functional synergy	HIF-1α activation is decoupled from the canonical Wnt/β-catenin pathway
Primary functional outcome	Promotes neurogenesis and improves neurological recovery	Synergistically promotes HBV transcription and replication	Promotes colorectal carcinogenesis (likely via alternative pathways, e.g., STAT3)

HBV: Hepatitis B virus; OSAS: Obstructive sleep apnea syndrome; HIF-1α: Hypoxia-inducible factor-1α; HBO: Hyperbaric oxygen; ROS: Reactive oxygen species; IH: Intermittent hypoxia; STAT3: Signal transducer and activator of transcription 3.