{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,7]],"date-time":"2026-05-07T18:15:14Z","timestamp":1778177714030,"version":"3.51.4"},"reference-count":72,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2026,5]]},"abstract":"<jats:sec>\n                    <jats:title>BACKGROUND:<\/jats:title>\n                    <jats:p>Knowledge of proteomic mechanisms explaining the link between psychosocial stress and cardiovascular disease is limited. This study aimed to (1) identify plasma proteins associated with psychosocial factors and (2) assess associational pathways between psychosocial factors, identified proteins, and incident cardiovascular disease events in a discovery cohort, JHS (Jackson Heart Study), and 2 replication cohorts, the CHS (Cardiovascular Health Study), and the MESA (Multi-Ethnic Study of Atherosclerosis).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS:<\/jats:title>\n                    <jats:p>\n                      JHS participants from exam 1 (2000\u20132004) with SomaScan 1.3k platform proteomics data were included (n=2143, mean age=55.3). Depressive symptoms and perceived stress scores were measured via the 20-item Center for Epidemiological Studies scale and an 8-item perceived stress scale adapted for the JHS, respectively. Multivariable linear regression models were used to test the association between psychosocial factors and plasma proteins, controlling for age, sex, proteomics batch, and estimated glomerular filtration rate. Bonferroni correction was used for multiple testing (\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      &lt;3.782\u00d710\n                      <jats:sup>\u22125<\/jats:sup>\n                      ) and meta-analyses were performed across cohorts. Mediation analyses with Cox proportional hazards models were used to evaluate potential proteomic pathways in the association between psychosocial factors and coronary heart disease, heart failure, and stroke in JHS.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS:<\/jats:title>\n                    <jats:p>\n                      Angiopoietin-2 (\n                      <jats:italic toggle=\"yes\">\u03b2<\/jats:italic>\n                      =0.014, SE=0.003,\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      &lt;0.001), contactin-5 (\n                      <jats:italic toggle=\"yes\">\u03b2<\/jats:italic>\n                      =\u22120.017, SE=0.003,\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      &lt;0.001), growth\/differentiation factor 15 or macrophage inhibitory cytokine 1 (\n                      <jats:italic toggle=\"yes\">\u03b2<\/jats:italic>\n                      =0.014, SE=0.002,\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      &lt;0.001), neural cell adhesion molecule 120 (\n                      <jats:italic toggle=\"yes\">\u03b2<\/jats:italic>\n                      =\u22120.016, SE=0.003,\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      &lt;0.001), and KYNU (kynureninase;\n                      <jats:italic toggle=\"yes\">\u03b2<\/jats:italic>\n                      =0.014, SE=0.003,\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      &lt;0.001) were each significantly associated with depressive symptoms, with angiopoietin-2, contactin-5, macrophage inhibitory cytokine 1, and neural cell adhesion molecule 120 replicating in CHS and MESA. Leukotriene A-4 hydrolase was associated with perceived stress (\n                      <jats:italic toggle=\"yes\">\u03b2<\/jats:italic>\n                      =0.0235, SE=0.005,\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      &lt;0.001). Macrophage inhibitory cytokine 1 partially accounted for the association between depressive symptoms and incident coronary heart disease in JHS (23%;\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      &lt;0.001).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS:<\/jats:title>\n                    <jats:p>Novel associations between psychosocial factors, plasma proteins, and cardiovascular disease were identified in JHS. Circulating proteomic profiles across 3 cardiovascular disease cohorts showed differences in protein concentrations by psychosocial measures. Future investigations should identify additional potentially targetable proteomic mechanisms by which psychosocial factors contribute to disease.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/atvbaha.125.324125","type":"journal-article","created":{"date-parts":[[2026,3,26]],"date-time":"2026-03-26T09:00:23Z","timestamp":1774515623000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":0,"title":["Plasma Proteins Associated With Psychosocial Factors and Heart Disease: The Jackson Heart Study"],"prefix":"10.1161","volume":"46","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6136-392X","authenticated-orcid":true,"given":"Sara N.","family":"O\u2019Brien","sequence":"first","affiliation":[{"name":"Department of Biostatistics (S.N.O.), University of North Carolina at Chapel Hill."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Madeline G.","family":"Gillman","sequence":"additional","affiliation":[{"name":"Department of Genetics (M.G.G., A.S.Z., L.M.R.), University of North Carolina at Chapel Hill."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4982-8154","authenticated-orcid":true,"given":"Michael D.","family":"Green","sequence":"additional","affiliation":[{"name":"Department of Population Health Sciences, Duke University School of Medicine, Durham, NC (M.D.G., L.M.G.)."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2576-7051","authenticated-orcid":true,"given":"Daniel E.","family":"Cruz","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School Teaching Hospital, Boston, MA (D.E.C., R.E.G., 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