{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T02:01:14Z","timestamp":1789956074770,"version":"4.0.1"},"reference-count":56,"publisher":"Wiley","license":[{"start":{"date-parts":[[2026,9,20]],"date-time":"2026-09-20T00:00:00Z","timestamp":1789862400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,9,20]],"date-time":"2026-09-20T00:00:00Z","timestamp":1789862400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["aocs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Lipids"],"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Remnant cholesterol and apolipoprotein B (\n                    <jats:styled-content style=\"fixed-case\">ApoB<\/jats:styled-content>\n                    ) are established contributors to coronary artery disease (\n                    <jats:styled-content style=\"fixed-case\">CAD<\/jats:styled-content>\n                    ), but their relationship with very\u2010large\n                    <jats:styled-content style=\"fixed-case\">VLDL<\/jats:styled-content>\n                    phospholipid composition remains uncertain. We evaluated whether genetically proxied\n                    <jats:styled-content style=\"fixed-case\">VLDL<\/jats:styled-content>\n                    phospholipid composition is linked to\n                    <jats:styled-content style=\"fixed-case\">CAD<\/jats:styled-content>\n                    through a connected remnant cholesterol\u2013\n                    <jats:styled-content style=\"fixed-case\">ApoB<\/jats:styled-content>\n                    axis. Summary\u2010level\n                    <jats:styled-content style=\"fixed-case\">GWAS<\/jats:styled-content>\n                    data were analyzed using network Mendelian randomization. Primary pairwise analyses used genome\u2010wide significant instruments (\n                    <jats:italic>P<\/jats:italic>\n                    \u2009&lt;\u20095\u2009\u00d7\u200910\n                    <jats:sup>\u22128<\/jats:sup>\n                    ) and inverse\u2010variance weighted random\u2010effects models, with weighted median,\n                    <jats:styled-content style=\"fixed-case\">MR<\/jats:styled-content>\n                    \u2010Egger,\n                    <jats:styled-content style=\"fixed-case\">MR<\/jats:styled-content>\n                    \u2010\n                    <jats:styled-content style=\"fixed-case\">PRESSO<\/jats:styled-content>\n                    , Steiger directionality, leave\u2010one\u2010out analyses, multivariable\n                    <jats:styled-content style=\"fixed-case\">MR<\/jats:styled-content>\n                    (\n                    <jats:styled-content style=\"fixed-case\">MVMR<\/jats:styled-content>\n                    ), and locus\u2010level colocalization as complementary analyses. Higher\n                    <jats:styled-content style=\"fixed-case\">VLDL<\/jats:styled-content>\n                    phospholipid ratio was associated with higher remnant cholesterol (\u03b2\u2009=\u20090.86, 95%\n                    <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>\n                    0.74\u20130.99) and higher\n                    <jats:styled-content style=\"fixed-case\">CAD<\/jats:styled-content>\n                    risk (\n                    <jats:styled-content style=\"fixed-case\">OR<\/jats:styled-content>\n                    \u2009=\u20091.80, 95%\n                    <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>\n                    1.54\u20132.11). Remnant cholesterol was associated with higher\n                    <jats:styled-content style=\"fixed-case\">ApoB<\/jats:styled-content>\n                    (\u03b2\u2009=\u20091.04, 95%\n                    <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>\n                    1.01\u20131.08), and\n                    <jats:styled-content style=\"fixed-case\">ApoB<\/jats:styled-content>\n                    with higher\n                    <jats:styled-content style=\"fixed-case\">CAD<\/jats:styled-content>\n                    risk (\n                    <jats:styled-content style=\"fixed-case\">OR<\/jats:styled-content>\n                    \u2009=\u20091.40, 95%\n                    <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>\n                    1.23\u20131.59). In\n                    <jats:styled-content style=\"fixed-case\">MVMR<\/jats:styled-content>\n                    models with adequate conditional instrument strength,\n                    <jats:styled-content style=\"fixed-case\">VLDL<\/jats:styled-content>\n                    phospholipid ratio remained associated with\n                    <jats:styled-content style=\"fixed-case\">CAD<\/jats:styled-content>\n                    after adjustment for remnant cholesterol (\n                    <jats:styled-content style=\"fixed-case\">OR<\/jats:styled-content>\n                    \u2009=\u20091.44, 95%\n                    <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>\n                    1.07\u20131.94) or\n                    <jats:styled-content style=\"fixed-case\">ApoB<\/jats:styled-content>\n                    (\n                    <jats:styled-content style=\"fixed-case\">OR<\/jats:styled-content>\n                    \u2009=\u20091.60, 95%\n                    <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>\n                    1.21\u20132.11), whereas their conditional effects were not independently significant. Remnant cholesterol and\n                    <jats:styled-content style=\"fixed-case\">ApoB<\/jats:styled-content>\n                    showed near\u2010complete genetic collinearity, limiting reliable separation of their independent effects. colocalization supported shared causal signals at multiple loci. The findings support a genetically connected VLDL\u2013remnant cholesterol\u2013ApoB lipid axis associated with CAD, but do not establish formal serial mediation. VLDL phospholipid composition may capture CAD\u2010relevant biology not fully explained by remnant cholesterol or ApoB alone.\n                  <\/jats:p>","DOI":"10.1002\/lipd.70085","type":"journal-article","created":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T01:26:24Z","timestamp":1789953984000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["<scp>VLDL<\/scp>\n                    Phospholipid Composition, Remnant Cholesterol,\n                    <scp>ApoB<\/scp>\n                    , and Coronary Artery Disease: A Network Mendelian Randomization Study"],"prefix":"10.1002","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7209-7716","authenticated-orcid":false,"given":"Haiyang","family":"Yu","sequence":"first","affiliation":[{"name":"College of Health Sciences Dezhou University  Dezhou 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China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2908-0289","authenticated-orcid":false,"given":"Dan","family":"Wang","sequence":"additional","affiliation":[{"name":"College of Health Sciences Dezhou University  Dezhou 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