Rapamycin reduced lung fibrosis and epithelial senescence in mice and A549 cells
In an abstract of a preclinical study, rapamycin suppressed an epithelial-mesenchymal transition marker, lowered SFN levels in A549 lung epithelial cells, and slowed fibrosis progression in bleomycin-challenged mice. These are animal and cell findings, not proven human benefits. [1]
Automatic summary · not editorially reviewed
The key findings
The authors screened approved drugs for EMT inhibition using bioinformatic algorithms and the human IPF dataset GSE53845, plus mouse lung tissue profiling. [1]
In A549 lung epithelial cells, rapamycin reduced SFN mRNA and protein, restored MDM2 nuclear translocation and accelerated ubiquitin-mediated p53 degradation. [1]
The abstract reports that this cascade blocked epithelial senescence and slowed fibrosis progression, and calls the evidence preclinical for drug repurposing. [1]
The source at a glance
- Study type / format
- Preclinical study abstract (bioinformatic screening, mouse model, cell assays)
- Population / context
- Bleomycin-challenged fibrotic mice and human A549 lung epithelial cells; human IPF dataset GSE53845 used for screening
- Summary based on
- Study abstract
- Publication status
- Preprint · peer-review status not confirmed
- Original publication
- September 28, 2026
Screening for EMT inhibitors in IPF datasets and mice
The authors aimed to screen already approved drugs that block epithelial-mesenchymal transition (EMT), a process they describe as an upstream driver of idiopathic pulmonary fibrosis (IPF). They used bioinformatic drug screening with LINCS/CMAP algorithms together with transcriptomic analysis of the human IPF dataset GSE53845. They also combined transcriptomic and proteomic profiling of lung tissue from bleomycin-challenged fibrotic mice. This was a preclinical, mechanism-focused search, not a study in patients.
Supporting source [1]
Rapamycin lowered SFN and slowed fibrosis in mice
Rapamycin (RAPA), described as a clinical immunosuppressant, was identified as a strong EMT suppressor. In A549 human lung epithelial cells, RAPA markedly reduced SFN mRNA and protein levels, restored movement of MDM2 into the nucleus, and accelerated ubiquitin-mediated degradation of p53. According to the abstract, this cascade blocked epithelial cell senescence and ultimately slowed progression of pulmonary fibrosis. The mouse model served for in vivo validation and A549 cells for in vitro functional assays.
Supporting source [1]
Preclinical evidence only; abstract without full text
The authors conclude that RAPA ameliorates pulmonary fibrosis and restrains epithelial senescence via the SFN-MDM2/p53 axis, and they call this reliable preclinical evidence for repurposing RAPA for IPF. The abstract reports no human trial; it states that no human-participant healthcare interventions were involved. It gives no sample sizes, follow-up times or effect estimates. This summary is based on the abstract only; the full text was not reviewed. Whether the same effects occur in people with IPF remains untested here.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. Findings come from bleomycin-challenged mice and A549 cells, not from people with IPF. No sample sizes, follow-up or effect estimates are reported.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Liu M, Du B, Xu Z, Cui X, Li Z, Huang L, Yuan J. · europepmc.org · September 28, 2026