mTOR mediates Wnt-induced epidermal stem cell exhaustion and aging
What this study shows
Wnt-induced mTOR activation drives epidermal stem-cell senescence; rapamycin rescues it.
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); 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 |
| Journal | Cell stem cell |
| Year | 2009 |
| Peer reviewed | Yes |
| Record last updated | 2026-10-01 |
| Source | DOI 10.1016/j.stem.2009.06.017 · PMID 19733540 · Free full text (PMC2939833) |
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 | Wnt1 overexpression; rapamycin rescue |
| Target | mTOR |
| Model | Mouse (epidermal stem cells) |
| Effect | Wnt→mTOR drives stem-cell senescence/exhaustion and hair loss; rapamycin reverses it |
| Dose | not stated |
| Sample size | n=25 mutant and wild-type littermates |
| Effect size | Wnt1 expression caused terminal differentiation of HF after 90 days, leading to progressive hair loss. |
| Limitations | No nuclear β-catenin staining could be observed, possibly due to strong membrane signal or limited nuclear β-catenin; further investigation is warranted on the contribution of particular Wnt1 receptors. |
In the Atlas
Related topics
Open questions that cite this study
- Cited as supporting evidence for the open question How much of rapamycin's healthspan benefit runs through fewer senescent cells?.
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