HIF-1α

Gene/Protein · 3 studies in the Atlas

Hypoxia-inducible factor 1-alpha, the main transcription factor for metabolic and angiogenic responses to low oxygen. Its output is partly mTORC1-dependent: in an Akt-driven mouse prostate model, mTOR inhibition reversed the lesions partly through HIF-1-dependent programmes (MAJ2004).

The low-oxygen alarm that also drives growth. The master switch a cell flips when oxygen runs short. It turns on genes that build new blood vessels and that shift the cell to making energy without oxygen. How much of this programme runs depends partly on mTORC1, so blocking mTOR can turn it down as well.

mTOR inhibition reverses Akt-driven prostate neoplasia partly through HIF-1-dependent pathways (MAJ2004). Note the arm this map does NOT contain: hypoxia → HIF-1α → REDD1 is real biology, but the corpus paper for the hypoxia arm (BRU2004) demonstrates REDD1 and TSC1/2 without establishing the HIF step, so that edge is not drawn.

TL;DR. HIF-1α appears in 3 curated studies in Oliver's mTOR Atlas: 3 in animal models. No study in people is recorded for it in the Atlas yet. It has 1 interaction in the curated pathway model.

In the pathway model

1 interaction in the curated mTOR pathway model. Each row is a claim with the evidence behind it; the evidence code is the kind of study, not its quality.

Interaction	Mechanism	Evidence	Studies
mTORC1 activates HIF-1α mechanism: signal-relay · this link in full · on the map table	In one specific setting (prostate cells), mTORC1 turns on a factor usually associated with low oxygen – here it's mTORC1 driving it, not the other way around. mTOR inhibition reverses Akt-driven prostate intraepithelial neoplasia partly through HIF-1-dependent pathways, placing HIF-1α downstream of mTORC1 in this setting. mTOR inhibition reverses Akt-driven prostate intraepithelial neoplasia partly through HIF-1-dependent pathways, placing HIF-1α downstream of mTORC1 in this setting. Holds under: Mouse prostate model with pharmacological mTOR inhibition; HIF-1α is one of several pathways implicated in the same experiment. plausible in people, not shown directly · emerging, few independent studies	A	MAJ2004

Evidence at a glance

Evidence	What it means	Studies
A	Animal model	3

No direct human evidence in the Atlas for this entity yet — everything below rests on animal or molecular work.

Studies

Year	Evidence	Study
2026	A	Rapamycin attenuates age-related atrial remodeling and fibrillation by targeting HIF-1α-mediated metabolic dysregulation. JIN2026B Dietary rapamycin reduced aging-induced atrial fibrillation susceptibility and atrial remodelling in D-galactose-aged mice, acting through mTOR-independent inhibition of HIF-1α plus restored mitochondrial function and insulin sensitivity.
2026	A	Salvianolic Acid B Enhances Motor Function Recovery after Spinal Cord Injury in Association with AKT/mTOR/HIF-1α Pathway Activation and Angiogenesis. YAO2026 Salvianolic acid B improved motor recovery, neuronal survival and angiogenesis after rat spinal cord injury in association with AKT/mTOR/HIF-1α activation; the effects were reversed by the AKT inhibitor capivasertib.
2004	A	mTOR inhibition reverses Akt-dependent prostate intraepithelial neoplasia through regulation of apoptotic and HIF-1-dependent pathways MAJ2004 mTOR inhibition (rapamycin/RAD001) reverses Akt-driven prostate intraepithelial neoplasia in mice.

Related entities

Spinal cord injuryCardiac aging 1 Rapamycin 1 Prostate cancer 1Atrial fibrillationPTEN 1 Akt/PKB 1Salvianolic acid B

Cite this page

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Barton, O. (2026). HIF-1α [Entity page]. In Oliver's mTOR Atlas [Data set]. https://mtor-atlas.org/gene/hif-1alpha/ · Dataset DOI 10.5281/zenodo.22059963

@misc{atlas_gene_hif_1alpha,
  author       = {Barton, Oliver},
  title        = {{Oliver's mTOR Atlas}: HIF-1α},
  howpublished = {Entity page in a data set},
  year         = {2026},
  url          = {https://mtor-atlas.org/gene/hif-1alpha/},
  doi          = {10.5281/zenodo.22059963}
}

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