HIF-1α

Embryonic HIF-1α is primarily involved in early embryonic development, whereas embryonic HIF-2α is required for later developmental stages.

Pathological hypoxia or aberrant HIF signaling drives pregnancy disorders including preeclampsia, fetal growth restriction, recurrent pregnancy loss, and heavy menstrual bleeding.

HIF-1α and HIF-2α have distinct spatial and temporal functions across reproductive stages.

Mouse genetics demonstrate that disruption of either HIF-1α or HIF-2α causes non-redundant defects in reproductive success, including failed implantation, placental insufficiency, and fetal lethality.

Maternal HIF-1α acts early in pregnancy to coordinate metabolic adaptation, endometrial regeneration, decidualization, angiogenic expansion, placental organization, and maternal immune tolerance.

HIF-1α and HIF-2α act as master regulators of early pregnancy-associated processes by sensing oxygen tension and orchestrating metabolism, angiogenesis, immune regulation, and tissue remodeling.

Defining distinct HIF-1α and HIF-2α roles supports development of therapies targeting hypoxia-responsive pathways in infertility and obstetric disease.

RUNX2 and HIF-1α are described as supporting each other or acting synergistically in osteosarcoma progression and therapy resistance.

RUNX2 and HIF-1α are implicated in tumour microenvironment alteration that promotes angiogenesis, metastasis, and therapy resistance in osteosarcoma.

HIF-1α overexpression is associated with decreased overall survival, decreased disease-free survival, reduced chemotherapy response, and increased tumour stage and metastasis in osteosarcoma.