ArticleFrontiers in medicine2026
Integrative multivariate genomic analysis reveals shared genetic determinants and druggable targets for vascular calcification.
Article in Frontiers in medicine, 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
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Vascular calcification (VC), characterized by calcium deposition in arterial walls, is a major risk factor for cardiovascular morbidity and mortality. While genome-wide association studies (GWAS) have identified susceptibility loci for specific vascular beds, such as coronary artery calcification (CAC) and abdominal aortic calcification (AAC), single-phenotype studies may overlook pleiotropic variants. This study aims to elucidate the shared genetic architecture of CAC and AAC and translate these findings into biological insights and potential therapeutic targets. Methods: We performed a multivariate genome-wide analysis integrating summary statistics for CAC and AAC from individuals of European ancestry. To prioritize candidate genes, we applied four complementary mapping strategies, including positional mapping, multivariate set-based association test, transcriptome-wide association study, and multi-marker analysis of genomic annotation. Findings were further characterized using tissue-specific expression profiling, Gene Ontology enrichment, and cell-type specificity analysis. Therapeutic potential and safety were subsequently evaluated using OpenTargets for druggability assessment and phenome-wide association studies (PheWAS) to assess horizontal pleiotropy. Finally, experimental validation was conducted to verify the genetic findings. Results: The multivariate analysis identified seven genome-wide significant loci. Cross-referencing the four gene-mapping strategies highlighted a consensus set of robust candidate genes, with Conclusion: This study demonstrates that CAC and AAC share a substantial genetic basis, reinforcing the concept of VC as a systemic pathological process driven by common mechanisms. By rigorously prioritizing candidate genes and mapping them to specific cell types, we provide a comprehensive genetic map of VC and highlight potentially safe targets for future therapeutic development.
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.