{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T08:04:14Z","timestamp":1789718654239,"version":"4.0.1"},"reference-count":79,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T00:00:00Z","timestamp":1789689600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Cardiovasc. Med."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Coronary artery disease (CAD) remains a leading cause of cardiovascular morbidity and mortality worldwide. Although traditional risk factors\u2014including dyslipidemia, hypertension, diabetes mellitus, obesity, and smoking\u2014account for a substantial proportion of CAD risk, they do not fully explain interindividual differences in disease onset, progression, or severity. Apolipoprotein E (ApoE) is a multifunctional protein involved in lipoprotein metabolism, inflammatory regulation, oxidative balance, endothelial function, and tissue repair. The APOE gene harbors three major alleles\u2014\n                      <jats:italic>\u03b5<\/jats:italic>\n                      2,\n                      <jats:italic>\u03b5<\/jats:italic>\n                      3, and\n                      <jats:italic>\u03b5<\/jats:italic>\n                      4\u2014generating six common genotypes. Among these, the\n                      <jats:italic>\u03b5<\/jats:italic>\n                      3\/\u03b54 genotype has been associated in several studies with an unfavorable lipid profile and increased susceptibility to CAD and premature CAD.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>\n                      This narrative review synthesizes current evidence on the association between the APOE\n                      <jats:italic>\u03b5<\/jats:italic>\n                      3\/\u03b54 genotype and CAD, with emphasis on lipid-mediated and non-lipid biological mechanisms, interactions with conventional cardiovascular risk factors, and potential implications for personalized cardiovascular prevention. Throughout the review, evidence obtained directly in \u03b53\/\u03b54 carriers is distinguished from evidence extrapolated from \u03b54-carrier, \u03b54\/\u03b54, or overall APOE-polymorphism analyses.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>A narrative literature search was conducted in PubMed, Embase, Scopus, and Web of Science from database inception to August 2026, using the terms \u201cApolipoprotein E,\u201d \u201cAPOE \u03b53\/\u03b54,\u201d \u201cAPOE polymorphism,\u201d \u201ccoronary artery disease,\u201d \u201cpremature coronary artery disease,\u201d \u201clipid metabolism,\u201d \u201catherosclerosis,\u201d and \u201ccardiovascular genetics.\u201d English-language original articles, narrative reviews, and meta-analyses relevant to the APOE \u03b53\/\u03b54 genotype and cardiovascular disease were included. Retrieved studies were classified by genotype contrast and by level of evidence (human observational, human interventional, or experimental).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Summary<\/jats:title>\n                    <jats:p>\n                      ApoE plays a central role in plasma lipoprotein transport and hepatic clearance of triglyceride-rich lipoprotein remnants. The\n                      <jats:italic>\u03b5<\/jats:italic>\n                      4 isoform has been associated with higher LDL cholesterol, apolipoprotein B, and remnant-lipoprotein concentrations, which may partly explain its association with coronary atherosclerosis. Beyond lipid transport, ApoE modulates macrophage activity, inflammatory signaling, oxidative stress, endothelial function, apoptosis, angiogenesis, and tissue repair. These non-lipid pathways derive predominantly from\n                      <jats:italic>in vitro<\/jats:italic>\n                      and animal models and remain unvalidated in human \u03b53\/\u03b54 carriers. Where adjusted, \u03b53\/\u03b53-referenced estimates are available, the effect size is modest, with odds ratios of approximately 1.5 for unselected CAD and 1.5\u20132.2 for premature coronary phenotypes.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      The APOE\n                      <jats:italic>\u03b5<\/jats:italic>\n                      3\/\u03b54 genotype may represent a genetic modifier of CAD risk, particularly when combined with traditional cardiovascular risk factors. Current evidence remains heterogeneous, and APOE genotyping should be regarded as a potential adjunctive marker and not a stand-alone risk prediction tool; this is distinct from its established diagnostic role in dysbetalipoproteinemia. Prospective studies integrating genetic, lipid, inflammatory, and imaging data are needed to clarify its incremental clinical value beyond LDL-C, apolipoprotein B, lipoprotein(a), and coronary artery calcium.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fcvm.2026.1885898","type":"journal-article","created":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T07:41:13Z","timestamp":1789717273000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Apolipoprotein E \u03b53\/\u03b54 and coronary artery disease: lipid and non-lipid mechanisms in personalized prevention \u2014 narrative review"],"prefix":"10.3389","volume":"13","author":[{"given":"Rodica","family":"Diaconu","sequence":"first","affiliation":[{"name":"CardioEcho Clinic","place":["Craiova, Romania"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vlad","family":"P\u0103dureanu","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Medicine and Pharmacy of Craiova","place":["Craiova, Romania"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R\u0103zvan Ilie","family":"Radu","sequence":"additional","affiliation":[{"name":"Intensive Cardiac Care Unit, Emergency Institute for Cardiovascular Diseases \u201cC. 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Iliescu\u201d","place":["Bucharest, Romania"]},{"name":"Department of Cardiology, University of Medicine and Pharmacy Carol Davila","place":["Bucharest, Romania"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria","family":"Iov\u0103nescu","sequence":"additional","affiliation":[{"name":"Department of Cardiology, University of Medicine and Pharmacy of Craiova","place":["Craiova, Romania"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Oana","family":"Mirea","sequence":"additional","affiliation":[{"name":"Department of Cardiology, University of Medicine and Pharmacy of Craiova","place":["Craiova, Romania"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Diana Ruxandra","family":"H\u0103d\u0103reanu","sequence":"additional","affiliation":[{"name":"Department of Cardiology, University of Medicine and Pharmacy of Craiova","place":["Craiova, Romania"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ionu\u0163","family":"Donoiu","sequence":"additional","affiliation":[{"name":"Department of Cardiology, University of Medicine and Pharmacy of Craiova","place":["Craiova, Romania"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,9,18]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"101622","DOI":"10.1016\/j.cpcardiol.2023.101622","article-title":"Global cardiovascular diseases death rate prediction","volume":"48","author":"Gaidai","year":"2023","journal-title":"Curr Probl Cardiol"},{"key":"B2","doi-asserted-by":"publisher","first-page":"192","DOI":"10.1001\/jamacardio.2022.3926","article-title":"Fundamental pathobiology of coronary atherosclerosis and clinical implications for chronic ischemic heart disease management\u2014the plaque hypothesis: a narrative review","volume":"8","author":"Stone","year":"2023","journal-title":"JAMA Cardiol"},{"key":"B3","doi-asserted-by":"publisher","first-page":"181","DOI":"10.1016\/j.tcm.2021.04.002","article-title":"Coronary heart disease risk: low-density lipoprotein and beyond","volume":"32","author":"Shaya","year":"2022","journal-title":"Trends Cardiovasc Med"},{"key":"B4","doi-asserted-by":"publisher","first-page":"687","DOI":"10.1038\/s41569-019-0202-5","article-title":"70-year Legacy of the framingham heart study","volume":"16","author":"Andersson","year":"2019","journal-title":"Nat Rev Cardiol"},{"key":"B5","doi-asserted-by":"publisher","first-page":"4063","DOI":"10.2174\/1381612825666190925163827","article-title":"A brief review of cardiovascular diseases, associated risk factors and current treatment regimes","volume":"25","author":"Flora","year":"2019","journal-title":"Curr Pharm Des"},{"key":"B6","doi-asserted-by":"publisher","first-page":"101","DOI":"10.1186\/s12872-024-03769-3","article-title":"Coronary artery disease incidence, risk factors, awareness, and medication utilization in a 10-year cohort study","volume":"24","author":"Sarebanhassanabadi","year":"2024","journal-title":"BMC Cardiovasc Disord"},{"key":"B7","doi-asserted-by":"publisher","first-page":"622","DOI":"10.1126\/science.3283935","article-title":"Apolipoprotein E: cholesterol transport protein with expanding role in cell biology","volume":"240","author":"Mahley","year":"1988","journal-title":"Science"},{"key":"B8","doi-asserted-by":"publisher","first-page":"165","DOI":"10.1016\/j.pathol.2018.11.002","article-title":"Apolipoprotein E in lipoprotein metabolism, health and cardiovascular disease","volume":"51","author":"Marais","year":"2019","journal-title":"Pathology"},{"key":"B9","doi-asserted-by":"publisher","first-page":"137","DOI":"10.1172\/JCI113849","article-title":"Changes of genetic apolipoprotein phenotypes caused by liver transplantation. 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