ArticleNature communications2025
Contribution of leukocyte telomere length to cardiovascular disease onset from genome-wide cross-trait analysis.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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
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Who cites it
4 citing papers in PubMed.
- Fibrosis and Perinatal Features Correlated with Telomere Shortening in Pediatric Metabolic Dysfunction-Associated Steatotic Liver Disease.Life (Basel, Switzerland) · 2026Article
- Article
- Genetic Determinants of Telomere Length and Their Role in Human Disease: Molecular Mechanisms and Underrepresented Populations' Perspectives.Biomedicines · 2026Review
- Prognostic value of baseline serum KL-6 for mortality risk in patients with idiopathic pulmonary fibrosis receiving antifibrotic therapy: A retrospective cohort study.Therapeutic advances in respiratory diseaseArticle
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
Telomere shortening is a well-established marker of cellular aging and genomic instability. While the relationship between leukocyte telomere length and cardiovascular diseases has long been of interest, their genetic interplay remains incompletely understood. In this study, we observe substantial genetic overlap beyond genome-wide correlations and identify a potential causal relationship between leukocyte telomere length and coronary artery disease. Specifically, we discover 248 pleiotropic loci, 22 of which show strong evidence of colocalization. Some shared loci implicate multiple pleiotropic genes across different trait pairs, including ALDH2, ACAD10, TMEM116, SH2B3 (all at 12q24.12), TMED6 (16q22.1), SERPINF1 (17p13.3), and XPO7 (8p21.3). Functional analysis highlights key pathways involved in DNA biosynthesis and telomere maintenance. Notably, SH2B3 is validated through proteome-wide Mendelian randomization analysis, suggesting its potential as a therapeutic target. Here we report the shared genetic basis between leukocyte telomere length and cardiovascular diseases, providing valuable insights into future therapeutic developments.
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