Akt/mTOR pathway is a crucial regulator of skeletal muscle hypertrophy and can prevent muscle atrophy in vivo
What this study shows
Akt/mTOR signalling is necessary and sufficient to drive skeletal-muscle hypertrophy and counteract atrophy in vivo.
At a glance
| Evidence type | A Animal model Marked A because it is an animal intervention or observation study measuring an organismal outcome (model: Mouse; muscle); the code names the system studied -- animal work can be rigorous and still not be human data. |
| Study type | 4 - Animal Study |
| Model system | Mouse; muscle |
| Journal | Nature cell biology |
| Year | 2001 |
| Peer reviewed | Yes |
| Record last updated | 2026-10-01 |
| Source | DOI 10.1038/ncb1101-1014 · PMID 11715023 |
Extracted findings
These fields were extracted from the paper with AI assistance and have not been checked against the source. Read them as a pointer into the paper, not as curated claims; where they disagree with the curated summary above, the curated summary stands.
| Intervention | Genetic/pharmacologic (Akt/mTOR; rapamycin) |
| Target | Akt / mTOR |
| Model | Mouse; muscle |
| Effect | Akt/mTOR is necessary and sufficient for skeletal muscle hypertrophy and prevents atrophy in vivo |
In the Atlas
Related topics
Links in the pathway map
- Supports Protein synthesis activates Muscle growth
- Supports Resistance exercise / mechanical load activates mTORC1
More studies on this topic
- Rapamycin administration in humans blocks the contraction-induced increase in skeletal muscle protein synthesis (2009)
- Translational control of long-lasting synaptic plasticity and memory (2009)
- IDH3 regulates citrate homeostasis to control metabolic fitness and venetoclax resistance of AML stem cells (2026)
- S6K1- and betaTRCP-mediated degradation of PDCD4 promotes protein translation and cell growth (2006)
Learn the biology
Want to understand the biology behind this study? → Growth Factor Signalling
Was this page useful?
Thank you. Your answer was counted anonymously.