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- W2904124790 endingPage "1810.e20" @default.
- W2904124790 startingPage "1796" @default.
- W2904124790 abstract "The 9p21.3 cardiovascular disease locus is the most influential common genetic risk factor for coronary artery disease (CAD), accounting for ∼10%-15% of disease in non-African populations. The ∼60 kb risk haplotype is human-specific and lacks coding genes, hindering efforts to decipher its function. Here, we produce induced pluripotent stem cells (iPSCs) from risk and non-risk individuals, delete each haplotype using genome editing, and generate vascular smooth muscle cells (VSMCs). Risk VSMCs exhibit globally altered transcriptional networks that intersect with previously identified CAD risk genes and pathways, concomitant with aberrant adhesion, contraction, and proliferation. Unexpectedly, deleting the risk haplotype rescues VSMC stability, while expressing the 9p21.3-associated long non-coding RNA ANRIL induces risk phenotypes in non-risk VSMCs. This study shows that the risk haplotype selectively predisposes VSMCs to adopt a cell state associated with CAD phenotypes, defines new VSMC-based networks of CAD risk genes, and establishes haplotype-edited iPSCs as powerful tools for functionally annotating the human genome." @default.
- W2904124790 created "2018-12-22" @default.
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- W2904124790 date "2018-12-01" @default.
- W2904124790 modified "2023-10-17" @default.
- W2904124790 title "Unveiling the Role of the Most Impactful Cardiovascular Risk Locus through Haplotype Editing" @default.
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- W2904124790 doi "https://doi.org/10.1016/j.cell.2018.11.014" @default.
- W2904124790 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6346426" @default.
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- W2904124790 hasPublicationYear "2018" @default.
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