In mouse models of atherosclerosis, smooth muscle cell (SMC)-specific disruption of a gene associated with coronary artery disease in human genome-wide association studies alters atherosclerotic plaque features by promoting SMC transition to an atherogenic phenotype.
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References
van der Harst, P. & Verweij, N. Identification of 64 novel genetic loci provides an expanded view on the genetic architecture of coronary artery disease. Circ. Res. 122, 433–443 (2020). Recent GWAS for CAD.
Miller, C. L. et al. Integrative functional genomics identifies regulatory mechanisms at coronary artery disease loci. Nat. Commun. 7, 12092 (2016). Application of genomic methods to identify causative CAD genetic variants.
Wirka, R. C. et al. Atheroprotective roles of smooth muscle cell phenotypic modulation and the TCF21 disease gene as revealed by single-cell analysis. Nat. Med. 25, 1280–1289 (2019). First application of single-cell and lesion analyses to study the mechanisms of atherosclerosis.
Kim, J. B. et al. Environment-sensing aryl hydrocarbon receptor inhibits the chondrogenic fate of modulated smooth muscle cells in atherosclerotic lesions. Circulation 142, 575–590 (2020). First characterization of SMC transition to a chondrocyte-like lineage.
Schunkert et al. Large-scale association analysis identifies 13 new susceptibility loci for coronary artery disease. Nat. Gen. 43, 333–338 (2011). First large GWAS meta-analysis to map CAD-associated loci.
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This is a summary of: Cheng, P. et al. Smad3 regulates smooth muscle cell fate and mediates adverse remodeling and calcification of the atherosclerotic plaque. Nat. Cardiovasc. Res. https://doi.org/10.1038/s44161-022-00042-8 (2022).
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Smooth muscle cell phenotypic transitions can modulate coronary artery disease risk. Nat Cardiovasc Res 1, 296–297 (2022). https://doi.org/10.1038/s44161-022-00053-5
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DOI: https://doi.org/10.1038/s44161-022-00053-5
