ArticleCommunications biology2024
Identification of shared genetic etiology of cardiovascular and cerebrovascular diseases through common cardiometabolic risk factors.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- The link between life satisfaction and outcome-wide health: evidence from the Canadian Longitudinal Study on Aging.American journal of epidemiology · 2026Article
- Precision medicine for atherosclerotic cardiovascular disease: Integrative genomics maps risk loci and AI-predicted functional consequences.Clinical and translational medicine · 2026Article
- Uncovering Novel Atrial Fibrillation Genetics Through Pleiotropic Overlap with Life's Essential 8.Biomedicines · 2026Article
- Rare coding variation and stroke heterogeneity in Saudi Arabia: an exome‑wide association study across severity, etiology, vascular territory, and early‑onset disease.BMC neurology · 2026Article
- Article
- Major depressive disorder (MDD) and the risks of mortality and hospitalization in the UK Biobank.BMC psychiatry · 2026Article
- Suggestive genome-wide associations with inflammatory biomarkers in an admixed population, including a missense variant in theFrontiers in immunology · 2026Article
- Plasma proteins and onset of atherosclerosis: integrating human plasma proteogenomics, transcriptomics and in vivo evidence.Journal of translational medicine · 2025Article
- Genetic and epigenetic architectures of stroke: Insights from GWAS to precision medicine.Neurochemistry international · 2025Review
- Genetic Pleiotropy and Causal Pathways Linking Glycemic Traits to Asthma: An Integrated Proteogenomic Investigation.Children (Basel, Switzerland) · 2025Article
- Breakfast Skipping Increases the Risk of Coronary Heart Disease and Myocardial Infarction: Evidence From the Mendelian Randomization Study.Food science & nutrition · 2025Article
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Authors and funding
13 authors.
Funding
Abstract
Cardiovascular diseases (CVDs) and cerebrovascular diseases (CeVDs) are closely related vascular diseases, sharing common cardiometabolic risk factors (RFs). Although pleiotropic genetic variants of these two diseases have been reported, their underlying pathological mechanisms are still unclear. Leveraging GWAS summary data and using genetic correlation, pleiotropic variants identification, and colocalization analyses, we identified 11 colocalized loci for CVDs-CeVDs-BP (blood pressure), CVDs-CeVDs-LIP (lipid traits), and CVDs-CeVDs-cIMT (carotid intima-media thickness) triplets. No shared causal loci were found for CVDs-CeVDs-T2D (type 2 diabetes) or CVDs-CeVDs-BMI (body mass index) triplets. The 11 loci were mapped to 12 genes, namely CASZ1, CDKN1A, TWIST1, CDKN2B, ABO, SWAP70, SH2B3, LRCH1, FES, GOSR2, RPRML, and LDLR, where both GOSR2 and RPRML were mapped to one locus. They were enriched in pathways related to cellular response to external stimulus and regulation of the phosphate metabolic process and were highly expressed in endothelial cells, epithelial cells, and smooth muscle cells. Multi-omics analysis revealed methylation of two genes (CASZ1 and LRCH1) may play a causal role in the genetic pleiotropy. Notably, these pleiotropic loci are highly enriched in the targets of antihypertensive drugs, which further emphasizes the role of the blood pressure regulation pathway in the shared etiology of CVDs and CeVDs.
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Registered trials
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