{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T05:25:16Z","timestamp":1787030716692,"version":"build-2736575974"},"reference-count":24,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T00:00:00Z","timestamp":1787011200000},"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                      <jats:italic>ABCA1<\/jats:italic>\n                      is a critical mediator of cholesterol efflux, and hypermethylation of its promoter may lead to transcriptional silencing. However, the relationship between\n                      <jats:italic>ABCA1<\/jats:italic>\n                      promoter methylation and the severity of coronary artery disease (CAD) remains poorly understood. This study aimed to explore whether\n                      <jats:italic>ABCA1<\/jats:italic>\n                      promoter methylation correlates with CAD severity and whether it could be used as a non-invasive epigenetic biomarker for auxiliary risk evaluation.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      This case-control study enrolled 80 consecutive patients with CAD (confirmed by coronary angiography) and 80 healthy controls from January 2025 to January 2026.\n                      <jats:italic>ABCA1<\/jats:italic>\n                      promoter methylation level was quantified using quantitative methylation-specific PCR. Associations with CAD diagnosis, Gensini scores, and clinical parameters were examined, with subgroup analyses by sex and age.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      <jats:italic>ABCA1<\/jats:italic>\n                      methylation levels were significantly elevated in the patients with CAD compared with the controls [median (IQR): 14.01% (8.11\u201319.28) vs. 9.99% (5.91\u201313.45),\n                      <jats:italic>P<\/jats:italic>\n                      \u2009&amp;lt;\u20090.05]. Logistic regression revealed that hypermethylation was an independent epigenetic correlate of CAD (OR\u2009=\u20091.087 per 1% increase, 95% CI: 1.010\u20131.170). This multivariable model was fully adjusted for age, sex, BMI, and serum lipid profile [total cholesterol (TC), triglycerides, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol (LDL-C), apolipoprotein A, and apolipoprotein B (ApoB)]. Among the patients with CAD, methylation level positively correlated with Gensini score (\n                      <jats:italic>\n                        r\n                        <jats:sub>s<\/jats:sub>\n                      <\/jats:italic>\n                      \u2009=\u20090.311,\n                      <jats:italic>P<\/jats:italic>\n                      \u2009&amp;lt;\u20090.05), TC (\n                      <jats:italic>\n                        r\n                        <jats:sub>s<\/jats:sub>\n                      <\/jats:italic>\n                      \u2009=\u20090.294,\n                      <jats:italic>P<\/jats:italic>\n                      \u2009&amp;lt;\u20090.05), LDL-C (\n                      <jats:italic>\n                        r\n                        <jats:sub>s<\/jats:sub>\n                      <\/jats:italic>\n                      \u2009=\u20090.284,\n                      <jats:italic>P<\/jats:italic>\n                      \u2009&amp;lt;\u20090.05), and ApoB (\n                      <jats:italic>\n                        r\n                        <jats:sub>s<\/jats:sub>\n                      <\/jats:italic>\n                      \u2009=\u20090.365,\n                      <jats:italic>P<\/jats:italic>\n                      \u2009&amp;lt;\u20090.01). In the overall cohort, methylation also correlated with ApoB (\n                      <jats:italic>\n                        r\n                        <jats:sub>s<\/jats:sub>\n                      <\/jats:italic>\n                      \u2009=\u20090.249,\n                      <jats:italic>P<\/jats:italic>\n                      \u2009&amp;lt;\u20090.05), age (\n                      <jats:italic>\n                        r\n                        <jats:sub>s<\/jats:sub>\n                      <\/jats:italic>\n                      \u2009=\u20090.297,\n                      <jats:italic>P<\/jats:italic>\n                      \u2009&amp;lt;\u20090.01), and female sex (\n                      <jats:italic>\n                        r\n                        <jats:sub>s<\/jats:sub>\n                      <\/jats:italic>\n                      \u2009=\u20090.803,\n                      <jats:italic>P<\/jats:italic>\n                      \u2009&amp;lt;\u20090.05).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      Peripheral blood\n                      <jats:italic>ABCA1<\/jats:italic>\n                      promoter methylation shows preliminary potential as a non-invasive epigenetic biomarker to assist auxiliary evaluation of coronary lesion severity, with particular promise in younger adults and women.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fcvm.2026.1876840","type":"journal-article","created":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T04:29:00Z","timestamp":1787027340000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Assessment of coronary artery disease severity via non-invasive detection of ABCA1 promoter 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