ArticleClinical epigenetics2023
Epigenetic aging in patients diagnosed with coronary artery disease: results of the LipidCardio study.
Article in Clinical epigenetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed, 10 citations in OpenAlex.
- Biological age acceleration and interaction with genetic predisposition in the risk of type 2 diabetes and coronary artery disease.GeroScience · 2026Article
- Methylation and algorithms in biological aging: a scoping review.Frontiers in aging · 2025Review
- Differentially Expressed Genes and Molecular Susceptibility to Human Age-Related Diseases.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionPeople age biologically at different rates. Epigenetic clock-derived DNA methylation age acceleration (DNAmAA) is among the most promising markers proposed to assess the interindividual differences in biological age. Further research is needed to evaluate the characteristics of the different epigenetic clock biomarkers available with respect to the health domains they reflect best.
methodsIn this study, we have analyzed 779 participants of the LipidCardio study (mean chronological age 69.9 ± 11.0 years, 30.6% women) who underwent diagnostic angiography at the Charité University Hospital in Berlin, Germany. DNA methylation age (DNAm age) was measured by methylation-sensitive single nucleotide primer extension (MS-SNuPE) and calculated with the 7-CpG clock. We compared the biological age as assessed as DNAmAA of participants with an angiographically confirmed coronary artery disease (CAD, n = 554) with participants with lumen reduction of 50% or less (n = 90) and patients with a normal angiogram (n = 135).
resultsParticipants with a confirmed CAD had on average a 2.5-year higher DNAmAA than patients with a normal angiogram. This association did not persist after adjustment for sex in a logistic regression analysis. High-density lipoprotein, low-density lipoprotein, triglycerides, lipoprotein (a), estimated glomerular filtration rate, physical activity, BMI, alcohol consumption, and smoking were not associated with DNAmAA.
conclusionThe association between higher DNAmAA and angiographically confirmed CAD seems to be mainly driven by sex.
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Registered trials
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