{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T08:45:03Z","timestamp":1792572303093,"version":"4.5.0"},"reference-count":40,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"13","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2026,7,7]]},"abstract":"<jats:sec xml:lang=\"en\">\n                    <jats:title>Background<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      Elevated soluble urokinase plasminogen activator receptor (suPAR) levels are associated with inflammation, immune activation, and major adverse cardiovascular events in coronary artery disease. Encoded by the\n                      <jats:italic toggle=\"no\">PLAUR<\/jats:italic>\n                      gene, suPAR levels are influenced by the rs4760 genetic variant. Whether proteomics\u2010based suPAR levels predict adverse outcomes in the general population remains unknown.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p xml:lang=\"en\">Proteomics\u2010based suPAR levels were measured using the Olink Immunoassay in 33\u2009963 UK Biobank participants without known coronary artery disease. Fine\u2010Gray and Cox proportional hazards models assessed associations between suPAR and major adverse cardiovascular events (primary outcome: cardiovascular mortality, nonfatal myocardial infarction, or stroke), cardiovascular mortality, and all\u2010cause mortality (secondary outcomes), after adjustment for demographic and clinical risk factors, hs\u2010CRP (high\u2010sensitivity C\u2010reactive protein), and the rs4760 variant. Incremental discrimination was evaluated using C\u2010statistics.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Results<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      Participants were aged 56.4 (SD, 8.2) years; 45% were men, and 93.4% were White. Over a median follow\u2010up of 14\u2009years (476\u2009177 person\u2010years), 10.7% experienced major adverse cardiovascular events, 2.6% experienced cardiovascular mortality, and 9.4% experienced all\u2010cause mortality. Each 1\u2010SD increment in proteomics\u2010based suPAR was associated with significantly higher risk of major adverse cardiovascular events (hazard ratio [HR], 3.2 [95% CI, 2.9\u20134.5]), cardiovascular mortality (HR, 5.9 [95% CI, 5.1\u20136.9]), and all\u2010cause mortality (HR, 5.0 [95% CI, 4.6\u20135.5]), independent of clinical risk factors and hs\u2010CRP. Additional adjustment for rs4760 did not attenuate these associations. Proteomics\u2010based suPAR significantly improved discrimination beyond clinical risk factors (C\u2010statistic: 0.719 versus 0.732;\n                      <jats:italic toggle=\"no\">P<\/jats:italic>\n                      &lt;0.001).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p xml:lang=\"en\">Proteomics\u2010based suPAR independently predicts adverse cardiovascular outcomes in the general population, beyond conventional risk factors, hs\u2010CRP, and genetic predisposition to elevated suPAR levels.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/jaha.125.047057","type":"journal-article","created":{"date-parts":[[2026,7,3]],"date-time":"2026-07-03T10:26:03Z","timestamp":1783074363000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":1,"title":["Proteomics\u2010Based Soluble Urokinase Plasminogen Activator Receptor Levels Are Associated With Adverse Cardiovascular Outcomes in the General Population: Insights From the UK Biobank"],"prefix":"10.1161","volume":"15","author":[{"ORCID":"https:\/\/orcid.org\/0009-0005-3787-2018","authenticated-orcid":false,"given":"Shaimaa M.","family":"Sakr","sequence":"first","affiliation":[{"name":"Emory University School of Medicine","place":["Atlanta"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8705-0462","authenticated-orcid":false,"given":"Jose R.","family":"Medina\u2010Inojosa","sequence":"additional","affiliation":[{"name":"Emory University School of Medicine","place":["Atlanta"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8918-7224","authenticated-orcid":false,"given":"Chang","family":"Liu","sequence":"additional","affiliation":[{"name":"Rollins School of Public Health, Emory 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