ReviewHerz2026
Age: a modifiable risk factor for cardiovascular disease?
Review in Herz, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Age is the strongest risk factor for cardiovascular disease, yet biological aging is increasingly recognized as a modifiable process. Animal studies over the past few decades have demonstrated that genetic, pharmacological, and dietary interventions can extend the healthspan and lifespan of animals by targeting conserved mechanisms of aging. Examining whether lifespan-extending interventions work in humans is challenging due to the long lifespan of our species. However, the development of biomarkers of biological aging or "aging clocks" has allowed for human trials where the rate of biological aging can be estimated. These surrogate markers now enable the first generation of human geroscience trials, in which interventions such as caloric restriction, rapamycin, taurine, plasma exchange, or nutritional strategies are evaluated for their ability to slow biological aging. Particularly relevant for cardiology are recently developed organ- and cell-specific aging clocks that estimate the biological age of the heart, vasculature, and cardiovascular cell types. These biomarkers may be suitable for improving cardiovascular risk prediction and providing surrogate outcomes for trials targeting cardiovascular aging. Together, these advances suggest that slowing biological aging could complement established cardiovascular prevention and treatment strategies in the future.
Indexed as
Identifiers
42970081What OpenQuestion holds
Registered trials
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.