{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,25]],"date-time":"2026-08-25T00:40:11Z","timestamp":1787618411876,"version":"build-2736575974"},"reference-count":51,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2025,9,10]],"date-time":"2025-09-10T00:00:00Z","timestamp":1757462400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01AG059501"],"award-info":[{"award-number":["R01AG059501"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","award":["HA 7512\/2\u20104"],"award-info":[{"award-number":["HA 7512\/2\u20104"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","award":["HA 7512\/2\u20101"],"award-info":[{"award-number":["HA 7512\/2\u20101"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100005971","name":"Deutsche Herzstiftung","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100005971","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000780","name":"European Commission","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000780","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Intern Med"],"published-print":{"date-parts":[[2025,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      High\u2010density lipoprotein (HDL) function, rather than its concentration, plays a crucial role in the development of coronary artery disease (CAD). Diminished HDL antioxidant properties, indicated by elevated oxidized HDL (nHDL\n                      <jats:sub>ox<\/jats:sub>\n                      ) and diminished paraoxonase\u20101 (PON\u20101) activity, may contribute to vascular dysfunction and inflammation. Data on these associations in CAD patients, including acute coronary syndrome (ACS), remain limited. The aim of this study is to assess the association of oxidized HDL with PON\u20101 activity, oxidized low\u2010density lipoprotein (LDL), vascular cell adhesion molecule\u20101 (VCAM\u20101), IL\u20106 levels, and nitric oxide (NO) production as markers of vascular health.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We assessed HDL function in three groups: 90 CAD patients, 90 healthy controls, and 90 ACS patients. HDL antioxidant function was measured using a validated biochemical assay to quantify oxidized HDL (nHDL\n                      <jats:sub>ox<\/jats:sub>\n                      ). Plasma PON\u20101 activity, oxidized LDL, VCAM\u20101, IL\u20106, and NO production were also evaluated.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      ACS patients had nHDL\n                      <jats:sub>ox<\/jats:sub>\n                      levels 140% higher than healthy controls (\n                      <jats:italic>p<\/jats:italic>\n                      \u00a0&lt;\u00a00.001). Higher nHDL\n                      <jats:sub>ox<\/jats:sub>\n                      levels were significantly linked to vascular inflammation, reflected by elevated VCAM\u20101 levels. Additionally, a reduced PON\u20101 activity indicates an impaired antioxidant protection in ACS patients. Finally, oxidized LDL levels were elevated, and NO production was reduced, suggesting impaired vascular function.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      HDL\n                      <jats:sub>ox<\/jats:sub>\n                      levels are highest in patients with ACS. Patients with stable CAD have higher levels than healthy controls. Correspondingly, the parameters of HDL function measured in this study, which all indicate a loss of HDL's atheroprotective function, correlate with these findings. Our study establishes a novel mechanistic pathway linking oxidized HDL to the presence of an ACS.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Clinical trial registration<\/jats:title>\n                    <jats:p>DRKS00014037<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/joim.70019","type":"journal-article","created":{"date-parts":[[2025,9,10]],"date-time":"2025-09-10T09:11:07Z","timestamp":1757495467000},"page":"464-477","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Oxidized high\u2010density lipoprotein associates with cardiometabolic dysfunction in coronary artery disease and acute coronary syndrome"],"prefix":"10.1111","volume":"298","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8157-9875","authenticated-orcid":false,"given":"Benjamin","family":"Sasko","sequence":"first","affiliation":[{"name":"Medical 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