Evidence map›Paper›PMID 42477095›Full record

ReviewNature aging2026

Positioning TERT at the apex of aging.

Ronald A DePinho

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature aging, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author.

Ronald A DePinhoDepartment of Cancer Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. RDePinho@mdanderson.org.ORCID http://orcid.org/0000-0002-5625-577X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aging is a biologically tractable process. Telomerase reverse transcriptase (TERT) has emerged as an upstream regulator coordinating several hallmarks of aging across preclinical models. Beyond maintaining telomeres, TERT influences mitochondrial health, epigenetic regulation, inflammation and stem cell function. Multiple translational strategies are being explored to modulate TERT. In mice and human cell models, restoration of physiological-range TERT expression characteristic of younger cells, or related telomere-focused interventions, has been associated with improvements in selected age-related phenotypes without a detectable increase in cancer. Simultaneously, human genetics links common variation in the TERT locus to increased risk of several cancers, underscoring the need for careful mechanistic and long-term safety evaluations. Together, mounting evidence indicates that TERT occupies an important position in aging biology with the potential to affect healthspan. This Perspective reviews current evidence for TERT's canonical and noncanonical roles and outlines a cautious therapeutic framework for evaluating TERT-directed geroprotective strategies.

Indexed as

AgingTelomeraseAnimalsEpigenesis, GeneticHumansMiceTelomereTelomeraseTERT protein, human

Identifiers

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.