ArticleAging cell2026
Estimating Vascular Age to Evaluate the Association Between Aging and Cardiovascular Disease.
Article in Aging cell, 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
11 authors.
Funding
Abstract
Vascular aging, characterized by progressive structural and functional deterioration of the vasculature, serves as a critical pathophysiological nexus between chronological aging and cardiovascular disease (CVD). This study establishes a quantitative vascular age model to decode individualized vascular senescence patterns, thereby enabling early identification of accelerated aging phenotypes for targeted intervention. We collected physical examination records from 2009 to 2019 and a total of 8578 participants aged 20-70 years were enrolled in this study. We constructed sex-specific basic vascular age models based on healthy individuals by Klemera-Doubal method and calculated the normalized cardiovascular age acceleration (NCAA, η) as an estimate of vascular aging status. The association between η and CVD risk were evaluated across subgroups. Furthermore, we developed expanded models by incorporating traditional CVD risk factors that were significantly associated with η index. Male with lower values of η, which meant relatively higher vascular aging velocity, had a higher risk of CVD adjusted by chronological age (HR = 1.21, 95% CI = 1.01-1.45). In subgroup analysis, η index exhibited age- and sex-specific associations with traditional CVD risk factors. After adding body mass index, fasting blood glucose, and triglycerides significantly related to η in male, the CVD prediction by expand η were improved in age-adjusted model (HR = 1.25, 95% CI = 1.04-1.50). The vascular age model emerges as a robust composite biomarker for CVD risk stratification. Our findings establish an evidence-based framework for precision prevention, prioritizing high-risk phenotypes for early intervention to mitigate CVD burden.
Indexed as
Identifiers
What Socratic 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 Socratic graph.