Study record
Telomerase gene therapy in a short-telomere pulmonary-fibrosis mouse model (Povedano et al., 2018)
Animal disease-model / mechanism study
Two caveats govern every page on this site. (1) Telomere length is a contested aging biomarker — it is measured differently by different methods, varies between tissues, and "longer" is not straightforwardly "healthier"; changing a telomere-length or telomerase-activity number in a trial is not the same as slowing human aging. (2) Activating telomerase is not risk-free — telomerase expression is low in many differentiated normal tissues, while some normal proliferating cells can express it. Cancer can also use telomere maintenance; the included human records do not resolve long-term cancer risk from pharmacological activation. Tellingly, the FDA-approved telomerase inhibitor — imetelstat (RYTELO, 2024) — inhibits telomerase to treat cancer (lower-risk MDS), the opposite direction from the anti-aging "activation" narrative.
○ Evidence tier 6 — Animal healthspan / disease-model / mechanism
Record verify: source publication identified; see evidence and limitations
| Design | Preclinical AAV-TERT gene-therapy study in a mouse pulmonary-fibrosis model |
| PMID | 29378675 |
| DOI | 10.7554/eLife.31299 |
| Citation status | Original publication identity matched by title, author and DOI; relevant full-text sections, results and limitations examined 2026-10-14. |
Five-qualifier claim
| Species / population | Mice with pulmonary fibrosis induced by low-dose bleomycin plus short telomeres (a short-telomere disease model). |
| Exposure, route, schedule | A tail-vein injection of AAV9-Tert: 100 μL at 2.5 × 10^13 viral genomes/mL, in the mouse model. Reporter-vector experiments showed preferential transduction of ATII cells. |
| Comparator / duration | AAV9-Empty comparison in the fibrosis experiment; lung-function, CT and tissue assessments from 1 to 8 weeks after vector treatment. AAV9-eGFP was used separately for cell-targeting measurements. |
| Endpoint / numeric result | In this model, lung-function and fibrosis measures improved, with 50% of treated mice having no detectable fibrotic lesions on the reported eight-week staining assessment. ATII cells showed improved relative telomere maintenance and less DNA damage. Lower apoptosis and senescence-marker measurements were also observed in lung tissue; those histological measurements did not distinguish all cell types. |
| What it did NOT establish | This short-telomere mouse disease-model experiment does not establish a human treatment benefit or human safety and did not measure lifespan extension. Eight-week tissue results cannot settle long-term tumor risk; the authors call for further work in cancer-prone or severely damaged tissue settings. |
Interventions
Primary reference
https://doi.org/10.7554/eLife.31299
Each identifier above was confirmed against the primary record; the citation status names the source and the date. An identifier that could not be confirmed is left empty and named as such in the record, never filled in from a secondary source.