Shared genetic architecture contributes to risk of major cardiovascular diseases

Jun Qiao, Lei Jiang (), Liuyang Cai, Minjing Chang, Can Wang, Rong Zhao, Shan Song, Yuhui Zhao, Miaoran Chen, Shifang Ding, Ning Tan, Pengcheng He, Sakthivel Sadayappan, Jinguo Xu (), Siim Pauklin (), Zhengbing Liu () and Yuliang Feng ()
Additional contact information
Jun Qiao: Southern University of Science and Technology
Lei Jiang: Southern Medical University
Liuyang Cai: Southern University of Science and Technology
Minjing Chang: Southern University of Science and Technology
Can Wang: Shanxi Medical University
Rong Zhao: South China University of Technology
Shan Song: Peking University First Hospital
Yuhui Zhao: Shanxi Precision Medical Engineering Research Center for Rheumatology
Miaoran Chen: Shanxi Precision Medical Engineering Research Center for Rheumatology
Shifang Ding: Southern Medical University
Ning Tan: Southern Medical University
Pengcheng He: Southern Medical University
Sakthivel Sadayappan: Cincinnati
Jinguo Xu: First Affiliated Hospital of Anhui Medical University
Siim Pauklin: Headington
Zhengbing Liu: Southern Medical University
Yuliang Feng: Southern University of Science and Technology

Nature Communications, 2025, vol. 16, issue 1, 1-16

Abstract: Abstract The extensive co-occurrence of cardiovascular diseases (CVDs), as evidenced by epidemiological studies, is supported by positive genetic correlations identified in comprehensive genetic investigations, suggesting a shared genetic basis. However, the precise genetic mechanisms underlying these associations remain elusive. By assessing genetic correlations, genetic overlap, and causal connections, we aim to shed light on common genetic underpinnings among major CVDs. Employing multi-trait analysis, we pursue diverse strategies to unveil shared genetic elements, encompassing SNPs, genes, gene sets, and functional categories with pleiotropic implications. Our study systematically quantifies genetic overlap beyond genome-wide genetic correlations across CVDs, while identifying a putative causal relationship between coronary artery disease (CAD) and heart failure (HF). We then pinpointed 38 genomic loci with pleiotropic influence across CVDs, of which the most influential pleiotropic locus is located at the LPA gene. Notably, 12 loci present high evidence of multi-trait colocalization and display congruent directional effects. Examination of genes and gene sets linked to these loci unveiled robust associations with circulatory system development processes. Intriguingly, distinct patterns predominantly driven by atrial fibrillation, coronary artery disease, and venous thromboembolism underscore the significant disparities between clinically defined CVD classifications and underlying shared biological mechanisms, according to functional annotation findings.

Date: 2025
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/s41467-025-62419-0 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:16:y:2025:i:1:d:10.1038_s41467-025-62419-0

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-025-62419-0

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().