Hypoxia
Low oxygen. Acts on mTORC1 transcriptionally, chiefly through REDD1 at the oxygen tensions used in these studies rather than through AMPK, so it is slower to engage and slower to release.
Not enough oxygen. Low oxygen levels. It reaches mTORC1 chiefly through a gene called REDD1 rather than through the AMPK energy-sensing route, so it's slower to switch the brake on and slower to release it again. Severe oxygen shortage does bring AMPK in as well.
REDD1 (DDIT4) induction by hypoxia is HIF-1-dependent in the wider literature, but the corpus paper for this arm (BRU2004) does not establish the HIF step, so the map draws hypoxia to REDD1 directly. Hypoxia also acts faster via AMPK and via direct effects on translation, so REDD1 is one arm, not the whole story.
TL;DR. Hypoxia appears in 2 curated studies in Oliver's mTOR Atlas: 1 in animal models; 1 at the molecular level (cells, biochemistry, structure). 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
| Interaction | Mechanism | Evidence | Studies |
|---|---|---|---|
| Hypoxia activates REDD1 (DDIT4) mechanism: transcriptional · this link in full · on the map table | Low oxygen switches on the gene for REDD1 over hours - slower than AMPK. REDD1 protein is short-lived, so the signal lasts only while low oxygen keeps the gene on. Low oxygen induces REDD1 transcriptionally over hours, slower than AMPK. REDD1 protein is short-lived, so the signal lasts only as long as hypoxia keeps the gene switched on. Low oxygen induces REDD1 transcriptionally over hours, slower than AMPK. REDD1 protein is short-lived, so the signal lasts only as long as hypoxia keeps the gene switched on. Holds under: Single-study edge in this corpus. plausible in people, not shown directly · emerging, few independent studies | M | BRU2004 |
Evidence at a glance
| Evidence | What it means | Studies |
|---|---|---|
| A | Animal model | 1 |
| M | Molecular — cells, biochemistry, structure | 1 |
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 | Role of Autophagy in Scleral Remodeling During Form-Deprivation Myopia WEN2026 Excess scleral autophagy links hypoxic stress to extracellular matrix remodelling in experimental myopia. In form-deprived guinea pigs, subconjunctival rapamycin made myopia worse and 3-MA alleviated it, while atropine slowed myopia and suppressed autophagy-related changes. AMPK/mTOR/P70S6K signalling was measured, but the paper does not establish it as the mediating route. |
| 2004 | M | Regulation of mTOR function in response to hypoxia by REDD1 and the TSC1/TSC2 tumor suppressor complex BRU2004 Hypoxia inhibits mTOR via REDD1-dependent activation of the TSC1/2 complex. |
Related entities
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