{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,12]],"date-time":"2026-09-12T03:00:38Z","timestamp":1789182038202,"version":"build-2803163510"},"reference-count":72,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"14","license":[{"start":{"date-parts":[[2024,10,1]],"date-time":"2024-10-01T00:00:00Z","timestamp":1727740800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[2024,10]]},"abstract":"<jats:sec>\n                    <jats:title>BACKGROUND:<\/jats:title>\n                    <jats:p>Activation of the immune system contributes to cardiovascular diseases. The role of human-specific long noncoding RNAs in cardioimmunology is poorly understood.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS:<\/jats:title>\n                    <jats:p>\n                      Single-cell sequencing in peripheral blood mononuclear cells revealed a novel human-specific long noncoding RNA called\n                      <jats:italic toggle=\"yes\">HEAT4<\/jats:italic>\n                      (heart failure\u2013associated transcript 4).\n                      <jats:italic toggle=\"yes\">HEAT4<\/jats:italic>\n                      expression was assessed in several in vitro and ex vivo models of immune cell activation, as well as in the blood of patients with heart failure (HF), acute myocardial infarction, or cardiogenic shock. The transcriptional regulation of\n                      <jats:italic toggle=\"yes\">HEAT4<\/jats:italic>\n                      was verified through cytokine treatment and single-cell sequencing. Loss-of-function and gain-of-function studies and multiple RNA\u2013protein interaction assays uncovered a mechanistic role of\n                      <jats:italic toggle=\"yes\">HEAT4<\/jats:italic>\n                      in the monocyte anti-inflammatory gene program.\n                      <jats:italic toggle=\"yes\">HEAT4<\/jats:italic>\n                      expression and function was characterized in a vascular injury model in NOD.CB17-Prkdc scid\/Rj mice.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS:<\/jats:title>\n                    <jats:p>\n                      <jats:italic toggle=\"yes\">HEAT4<\/jats:italic>\n                      expression was increased in the blood of patients with HF, acute myocardial infarction, or cardiogenic shock.\n                      <jats:italic toggle=\"yes\">HEAT4<\/jats:italic>\n                      levels distinguished patients with HF from people without HF and predicted all-cause mortality in a cohort of patients with HF over 7 years of follow-up. Monocytes, particularly anti-inflammatory CD16\n                      <jats:sup>+<\/jats:sup>\n                      monocytes, which are increased in patients with HF, are the primary source of\n                      <jats:italic toggle=\"yes\">HEAT4<\/jats:italic>\n                      expression in the blood.\n                      <jats:italic toggle=\"yes\">HEAT4<\/jats:italic>\n                      is transcriptionally activated by treatment with anti-inflammatory interleukin-10.\n                      <jats:italic toggle=\"yes\">HEAT4<\/jats:italic>\n                      activates anti-inflammatory and inhibits proinflammatory gene expression. Increased\n                      <jats:italic toggle=\"yes\">HEAT4<\/jats:italic>\n                      levels result in a shift toward more CD16\n                      <jats:sup>+<\/jats:sup>\n                      monocytes.\n                      <jats:italic toggle=\"yes\">HEAT4<\/jats:italic>\n                      binds to S100A9, causing a monocyte subtype switch, thereby reducing inflammation. As a result,\n                      <jats:italic toggle=\"yes\">HEAT4<\/jats:italic>\n                      improves endothelial barrier integrity during inflammation and promotes vascular healing after injury in mice.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS:<\/jats:title>\n                    <jats:p>\n                      These results characterize a novel endogenous anti-inflammatory pathway that involves the conversion of monocyte subtypes into anti-inflammatory CD16\n                      <jats:sup>+<\/jats:sup>\n                      monocytes. The data identify a novel function for the class of long noncoding RNAs by preventing protein secretion and suggest long noncoding RNAs as potential targets for interventions in the field of cardioimmunology.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/circulationaha.124.069315","type":"journal-article","created":{"date-parts":[[2024,7,15]],"date-time":"2024-07-15T05:00:39Z","timestamp":1721019639000},"page":"1101-1120","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":9,"title":["Novel Long Noncoding RNA\n                    <i>HEAT4<\/i>\n                    Affects Monocyte Subtypes, Reducing Inflammation and Promoting Vascular Healing"],"prefix":"10.1161","volume":"150","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0273-3614","authenticated-orcid":true,"given":"Jasmin M.","family":"Kneuer","sequence":"first","affiliation":[{"name":"Klinik und Poliklinik f\u00fcr Kardiologie, Universit\u00e4tsklinikum Leipzig, Germany (J.M.K., I.A.G., M.W., S.E., T.M., M.N.M.-W., A.K., K.E.K., V.F., S.G., U.L., J.-N.B.)."},{"name":"Central German Heart Alliance (J.M.K., I.A.G., M.W., S.E., T.M., M.N.M.-W., A.K., K.E.K., V.F., S.G., H.T., U.L., J.-N.B.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ignacy A.","family":"Grajek","sequence":"additional","affiliation":[{"name":"Klinik und Poliklinik f\u00fcr Kardiologie, Universit\u00e4tsklinikum Leipzig, Germany (J.M.K., I.A.G., M.W., S.E., T.M., M.N.M.-W., A.K., K.E.K., V.F., S.G., U.L., J.-N.B.)."},{"name":"Central German Heart Alliance (J.M.K., I.A.G., M.W., S.E., T.M., M.N.M.-W., A.K., K.E.K., V.F., S.G., H.T., U.L., J.-N.B.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Melanie","family":"Winkler","sequence":"additional","affiliation":[{"name":"Klinik und Poliklinik f\u00fcr Kardiologie, Universit\u00e4tsklinikum Leipzig, Germany (J.M.K., I.A.G., M.W., S.E., T.M., M.N.M.-W., A.K., 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