ArticleClinical epigenetics2026
Changes of DNA methylation in smokers and ex-smokers referred for coronary angiography. Results from the LURIC study.
Article in Clinical epigenetics, 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
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTobacco smoking remains a major global health burden and is a leading risk factor for cardiovascular disease and cancer. Accumulating evidence suggests that tobacco smoke induces widespread alterations in DNA methylation, which may contribute to smoking-related morbidity and mortality.
methodsThe Ludwigshafen Risk and Cardiovascular Health (LURIC) study is a monocentric prospective cohort including 3316 patients referred for coronary angiography. Genome-wide DNA methylation was assessed in 2423 participants using the Illumina HumanMethylationEPIC BeadChip. A discovery-replication design was applied (discovery n = 1262; replication n = 1161). Associations between smoking status (never/former vs. current) and CpG-specific methylation levels were evaluated using multivariable linear regression models. Cox proportional hazards models were used to assess associations with all-cause and cardiovascular mortality. Mediation was examined within a counterfactual framework using natural effect models.
resultsIn the discovery sample, 14,403 CpG sites were significantly associated with smoking after false-discovery-rate correction (differentially methylated probes, DMPs). Of these, 3,000 were replicated in the independent sample at an FDR-adjusted p value < 0.05. In random-effect meta-analysis of both samples, 24,930 DMPs remained significant after multiple testing correction, of which 11,907 had not been reported in the largest published smoking EWAS to date. Among former smokers, a subset of DMPs remained differentially methylated more than 10 years after smoking cessation, indicating long-term persistence of smoking-associated epigenetic alterations. A CpG score constructed from mortality-associated DMPs was strongly associated with all-cause mortality. Inclusion of this score in Cox regression models attenuated the association between smoking status and mortality. Mediation analysis demonstrated a statistically significant natural indirect effect of smoking on all-cause mortality via the CpG score.
conclusionsTobacco smoking is associated with widespread, exposure-dependent alterations in DNA methylation, many of which persist for years after cessation. These epigenetic changes are strongly linked to mortality risk and may represent an important biological pathway underlying the association between smoking and adverse health outcomes.
Indexed as
Identifiers
What 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.