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 is silenced in most somatic cells and reactivated in most cancers, so its activation raises an unresolved cancer-risk question. Tellingly, the only FDA-approved telomerase drug — 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
| Design | Preclinical AAV-TERT gene-therapy study in a mouse pulmonary-fibrosis model |
| DOI | 10.7554/eLife.31299 |
| Citation status | doi verified via Crossref 2026-07-12 (eLife 2018;7:e31299, Povedano, Martinez, Serrano, Tejera, Gomez-Lopez, Bobadilla, Flores, Bosch, Blasco, 'Therapeutic effects of telomerase in mice with pulmonary fibrosis induced by damage to the lungs and short telomeres'). PMID not separately fetched (DOI is the confirmed primary identifier). |
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 | AAV9 vector expressing TERT (AAV9-Tert), which preferentially targets regenerative alveolar type-II cells. |
| Comparator / duration | AAV9 control vector; assessed 1–8 weeks after treatment. |
| Endpoint / numeric result | AAV9-Tert improved lung function and lowered inflammation and fibrosis, with fibrosis improvement or resolution by 8 weeks; longer telomeres and reduced DNA damage, apoptosis and senescence in ATII cells. |
| What it did NOT establish | A mouse disease-model result (proof-of-principle), not human evidence and not a lifespan endpoint. The human cancer-risk question is unresolved. |
Interventions
Primary reference
https://doi.org/10.7554/eLife.31299
Exact identifier confirmed against the primary record via Crossref/ClinicalTrials.gov where stated in the citation status; anything marked needs_primary_fulltext is not yet confirmed.