Oxidative phosphorylation
Mitochondrial respiratory capacity, supported by mTORC1.
Burning fuel for energy. Burning fuel for energy.
Controlled through a YY1–PGC-1α transcriptional programme (CUN2007) and 4E-BP-dependent translation of respiratory components (MOR2013). Adipose Raptor knockout RAISES respiration (POL2008), which runs against this direction and is carried here as conflicting evidence, not as genetic confirmation.
TL;DR. Oxidative phosphorylation appears in 3 curated studies in Oliver's mTOR Atlas: 1 in people (1 human study); 2 at the molecular level (cells, biochemistry, structure). It has 1 interaction in the curated pathway model.
In the pathway model
| Interaction | Mechanism | Evidence | Studies |
|---|---|---|---|
| mTORC1 activates Oxidative phosphorylation mechanism: signal-relay · this link in full · on the map table | mTORC1 boosts how much energy mitochondria can produce, through both gene activation and protein-building. One mouse experiment points the other way – removing mTORC1 from fat tissue RAISED respiration – so this direction is not settled in a living animal. mTORC1 raises mitochondrial respiratory capacity through a YY1–PGC-1α transcriptional programme and through 4E-BP-dependent translation of respiratory components. mTORC1 raises mitochondrial respiratory capacity through a YY1–PGC-1α transcriptional programme and through 4E-BP-dependent translation of respiratory components. Holds under: Effect size varies strongly by tissue; the transcriptional and translational arms have not been cleanly separated in vivo. OVERLAP (audit 2026-09-04): this edge and MTORC1-MITO assert overlapping biology from overlapping citations (CUN2007, MOR2013) at different tiers and different consensus levels. Read them together; they are not independent support. plausible in people, not shown directly · emerging, few independent studies | M | CUN2007, MOR2013 conflicting: POL2008 |
Evidence at a glance
| Evidence | What it means | Studies |
|---|---|---|
| H | Human study | 1 |
| M | Molecular — cells, biochemistry, structure | 2 |
Studies
| Year | Evidence | Study |
|---|---|---|
| 2026 | H | Sexual Dimorphism in Placental mTORC1 Signaling, Amino Acid Transport, and Mitochondrial Respiration at Term. SHIMADA2026 In 46 term placentas, male placentas showed higher mTORC1 signalling (increased S6RP phosphorylation, reduced 4E-BP1), greater System A amino acid transport and higher mitochondrial respiratory capacity than female placentas, and male pregnancies had a higher birth-weight-to-placental-weight ratio. Observational: a cross-sectional association at a single timepoint, with no intervention and no randomisation, so the direction of the relationship between mTORC1 signalling and growth is not established here and residual confounding by maternal and obstetric factors cannot be excluded. |
| 2013 | M | mTORC1 controls mitochondrial activity and biogenesis through 4E-BP-dependent translational regulation MOR2013 mTORC1 controls mitochondrial biogenesis and activity through 4E-BP-dependent translation. |
| 2007 | M | mTOR controls mitochondrial oxidative function through a YY1-PGC-1alpha transcriptional complex CUN2007 Showed mTOR isn't just about building proteins - it also runs the cell's POWER plants. mTORC1 drives mitochondrial gene expression and oxygen consumption through a YY1-PGC-1alpha transcriptional program; block mTOR with rapamycin and mitochondrial output falls. Explains part of why mTOR inhibition reshapes metabolism. |
Related entities
Was this page useful?
Thank you. Your answer was counted anonymously.