ArticleClinical epigenetics2025
Epigenetic age acceleration in Turner and Klinefelter syndrome: Correlations with clinical aging markers.
Article in Clinical epigenetics, 2025. 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
5 authors.
Funding
Abstract
backgroundThe sex chromosome aneuploidies Turner syndrome (45,X; TS) and Klinefelter syndrome (47,XXY; KS) are associated with aging-related comorbidities, reduced life expectancy and genome-wide DNA methylation changes. This indicates that biological aging, reflecting physiological function rather than chronological age, is increased in both syndromes. To investigate whether DNA methylation patterns linked to physiological decline could contribute to the comorbidity patterns and reduced lifespan in TS and KS, we applied so-called epigenetic clocks to DNA methylation data from cohorts of TS (n = 57) compared to female controls (n = 33) and KS (n = 65) compared to male controls (n = 63). Additionally, we evaluated correlations between epigenetic age and clinical variables, aiming to identify clinical aging markers in TS and KS.
resultsComparing TS to female controls, all epigenetic clocks indicated advanced biological aging. Comparing KS to male controls, less evidence was observed although some epigenetic clocks indicated accelerated biological aging. Considering estrogen replacement therapy in TS, some epigenetic clocks found that treatment reduced biological age in TS. Correlating epigenetic clocks to clinical variables, several unfavorable outcomes-mainly related to body composition-correlated with age in controls. In TS, and in some cases KS, these correlations were diminished. In TS and KS, we instead found correlations between body composition and the rate of aging.
conclusionWe demonstrated that biological aging was clearly increased in sex chromosome aneuploidies, especially TS, potentially contributing to the severely reduced lifespan. Additionally, unfavorable changes in body composition, common in both TS and KS, and in particular in the presence of hypogonadism, could result in accelerated aging-or be the result thereof.
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.