ArticleAmerican journal of human genetics2023
Dissecting the polygenic basis of atherosclerosis via disease-associated cell state signatures.
Article in American journal of human genetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 45 citations in OpenAlex.
- Early atherogenesis: In search of etiology.International journal of cardiology. Cardiovascular risk and prevention · 2026Review
- Serum/glucocorticoid-regulated kinase 1 regulates vascular inflammation in atherosclerosis.Acta pharmacologica Sinica · 2026Article
- Cell-type-specific polygenic risk scores reveal adipocyte-related interactions with lipids in coronary artery disease.medRxiv : the preprint server for health sciences · 2026Article
- Translating genome-wide association studies at multiple scales: Drug target prioritization, cellular architectures, and organ imaging.Cell genomics · 2026Review
- Functionally informed annotation influences pathway-specific polygenic risk and disease inference in Alzheimer's disease.medRxiv : the preprint server for health sciences · 2026Article
- Female-Biased VSMC GRNs Predict MYH9 as Regulator of Fibrous Plaque Phenotype.Circulation research · 2026Article
- Vascular smooth muscle cell state trajectories mediate molecular mechanisms of coronary disease risk.Nature communications · 2026Article
- Fitness Training for γδ T cells in mouse and human atherosclerosis takes place in plaques and artery tertiary lymphoid organs.Genome medicine · 2026Article
- Multi-omics data integration from patients with carotid stenosis illuminates key molecular signatures of atherosclerotic instability.Genome medicine · 2026Article
- Non-remnant triglyceride-rich lipoproteins due to lipoprotein lipase deficiency increase atherosclerosis in mice.Nature communications · 2026Article
- Single-cell to pre-clinical evaluation of Trem2, Folr2, and Slc7a7 as macrophage-associated biomarkers for atherosclerosis.Cardiovascular research · 2025Article
- Review
- YAP/TAZ deletion in vascular smooth muscle cells mirrors atherosclerosis-associated transcriptional programs.Journal of molecular and cellular cardiology plus · 2025Article
- Mapping atherogenesis mechanisms in smooth muscle cells by targeting genes linked to coronary artery disease.iScience · 2025Article
- Multi-omic derived cell-type specific Alzheimer disease polygenic risk scores.Neurobiology of aging · 2025Article
- Polygenicity at the pathway level for anorexia nervosa.medRxiv : the preprint server for health sciences · 2025Article
- MicroRNA gene dynamics in immune cell subpopulations during aging and atherosclerosis disease development at single-cell resolution.Genome medicine · 2025Article
- The loss of microRNA-26b promotes aortic calcification through the regulation of cell-specific target genes.Cardiovascular research · 2025Article
- Distinct inflammatory pathways shape atherosclerosis in different vascular beds.European heart journal · 2025Review
- Macrophage WEE1 Directly Binds to and Phosphorylates NF-κB p65 Subunit to Induce Inflammatory Response and Drive Atherosclerosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
19 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Coronary artery disease (CAD) is a pandemic disease where up to half of the risk is explained by genetic factors. Advanced insights into the genetic basis of CAD require deeper understanding of the contributions of different cell types, molecular pathways, and genes to disease heritability. Here, we investigate the biological diversity of atherosclerosis-associated cell states and interrogate their contribution to the genetic risk of CAD by using single-cell and bulk RNA sequencing (RNA-seq) of mouse and human lesions. We identified 12 disease-associated cell states that we characterized further by gene set functional profiling, ligand-receptor prediction, and transcription factor inference. Importantly, Vcam1+ smooth muscle cell state genes contributed most to SNP-based heritability of CAD. In line with this, genetic variants near smooth muscle cell state genes and regulatory elements explained the largest fraction of CAD-risk variance between individuals. Using this information for variant prioritization, we derived a hybrid polygenic risk score (PRS) that demonstrated improved performance over a classical PRS. Our results provide insights into the biological mechanisms associated with CAD risk, which could make a promising contribution to precision medicine and tailored therapeutic interventions in the future.
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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.