{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T18:22:13Z","timestamp":1785435733530,"version":"3.56.0"},"reference-count":63,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","license":[{"start":{"date-parts":[[2025,10,1]],"date-time":"2025-10-01T00:00:00Z","timestamp":1759276800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circ: Genomic and Precision Medicine"],"published-print":{"date-parts":[[2025,10]]},"abstract":"<jats:sec>\n                    <jats:title>BACKGROUND:<\/jats:title>\n                    <jats:p>Previous studies have suggested that the associations between ambient air pollution and atherosclerotic cardiovascular diseases (ASCVD) differ by genotype. A genome-wide approach provides a more comprehensive understanding of this relationship on a genomic scale.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS:<\/jats:title>\n                    <jats:p>\n                      Using data from \u2248300\u2009000 UK Biobank participants, we conducted a genome-wide interaction analysis on 10\u2009745\u2009802 variants. We examined the interactions between fine particulate matter (PM\n                      <jats:sub>2.5<\/jats:sub>\n                      ) and genetic variants across 3 ASCVD subtypes: coronary artery disease, ischemic stroke, and peripheral artery disease. A polygenic risk score was constructed, and functional annotation identified potential genes at loci interacting with air pollution. In vivo studies explored how genome-wide interaction analysis-identified genes interacting with PM\n                      <jats:sub>2.5<\/jats:sub>\n                      might contribute to atherosclerotic plaque progression.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS:<\/jats:title>\n                    <jats:p>\n                      During 12.55 years of follow-up, 42\u2009696 ASCVD events were observed. Genome-wide interaction analysis identified 12 loci shared across the ASCVD subtypes related to PM\n                      <jats:sub>2.5<\/jats:sub>\n                      exposure. Functional annotation suggested these loci and colocalized genes are involved in pathways such as cell-cell adhesion, deoxyribonucleotide biosynthesis, RNA metabolism, and calcium homeostasis. High genetic risk combined with PM\n                      <jats:sub>2.5<\/jats:sub>\n                      exposure was associated with coronary artery disease, ischemic stroke, and peripheral artery disease, with hazard ratios and 95% CIs of 1.35 (1.32\u20131.37), 1.53 (1.47\u20131.58), and 1.68 (1.62\u20131.75), respectively. Animal studies confirmed that adenosine kinase gene expression might interact with PM\n                      <jats:sub>2.5<\/jats:sub>\n                      , potentially influencing atherosclerotic plaque development through inflammation.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS:<\/jats:title>\n                    <jats:p>\n                      Our study identified genome-wide loci interacting with PM\n                      <jats:sub>2.5<\/jats:sub>\n                      and linked adenosine kinase expression in response to PM\n                      <jats:sub>2.5<\/jats:sub>\n                      exposure to the formation of atherosclerotic plaques, highlighting potential pathways that connect PM\n                      <jats:sub>2.5<\/jats:sub>\n                      to ASCVD.\n                    <\/jats:p>\n                  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