ArticleCommunications biology2024
Protein interaction networks in the vasculature prioritize genes and pathways underlying coronary artery disease.
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 5 papers.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Targeting protein protein interactions and their modulators to enable new therapeutic strategies for human diseases.NPJ systems biology and applications · 2026Review
- HSP90AA1 Facilitates Vascular Calcification in Chronic Kidney Disease Involving Chaperone-Mediated Autophagy.Biomedicines · 2026Article
- DNA-damage-associated protein co-expression network in cardiomyocytes informs on tolerance to genetic variation and disease.iScience · 2025Article
- Serum proteomic profiling reveals potential predictive indicators for coronary artery calcification in stable ischemic heart disease.Journal of molecular histology · 2025Article
- Comprehensive analysis of non-coding RNA-mediated endothelial cell-specific regulatory circuits in coronary artery disease risk.Frontiers in genetics · 2025Article
Corrections and comments
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Authors and funding
17 authors at 2 institutions in 3 countries.
Funding
Abstract
Population-based association studies have identified many genetic risk loci for coronary artery disease (CAD), but it is often unclear how genes within these loci are linked to CAD. Here, we perform interaction proteomics for 11 CAD-risk genes to map their protein-protein interactions (PPIs) in human vascular cells and elucidate their roles in CAD. The resulting PPI networks contain interactions that are outside of known biology in the vasculature and are enriched for genes involved in immunity-related and arterial-wall-specific mechanisms. Several PPI networks derived from smooth muscle cells are significantly enriched for genetic variants associated with CAD and related vascular phenotypes. Furthermore, the networks identify 61 genes that are found in genetic loci associated with risk of CAD, prioritizing them as the causal candidates within these loci. These findings indicate that the PPI networks we have generated are a rich resource for guiding future research into the molecular pathogenesis of CAD.
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Registered trials
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