{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,24]],"date-time":"2026-10-24T00:50:20Z","timestamp":1792803020821,"version":"4.5.0"},"reference-count":30,"publisher":"Oxford University Press (OUP)","issue":"11","license":[{"start":{"date-parts":[[2019,11,11]],"date-time":"2019-11-11T00:00:00Z","timestamp":1573430400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"name":"StrukMed and Clinical Scientist"},{"name":"German Federal Ministry of Education and Research"},{"DOI":"10.13039\/501100002347","name":"BMBF","doi-asserted-by":"publisher","award":["01 KG 1001"],"award-info":[{"award-number":["01 KG 1001"]}],"id":[{"id":"10.13039\/501100002347","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001659","name":"German Research Foundation","doi-asserted-by":"crossref","award":["DFG, HI 842\/4-3"],"award-info":[{"award-number":["DFG, HI 842\/4-3"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"crossref"}]},{"name":"DFG Clinical Research Group","award":["KFO 311"],"award-info":[{"award-number":["KFO 311"]}]},{"name":"DFG Clinical Research Group","award":["HI 842\/10-1"],"award-info":[{"award-number":["HI 842\/10-1"]}]},{"name":"DFG Clinical Research Group","award":["RI 2531\/2-1"],"award-info":[{"award-number":["RI 2531\/2-1"]}]},{"name":"State of Lower Saxony and the Volkswagen Foundation","award":["VWZN3009"],"award-info":[{"award-number":["VWZN3009"]}]},{"DOI":"10.13039\/501100002996","name":"Dutch Heart Foundation","doi-asserted-by":"crossref","award":["2012T47"],"award-info":[{"award-number":["2012T47"]}],"id":[{"id":"10.13039\/501100002996","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100010663","name":"European Research Council","doi-asserted-by":"publisher","award":["ERC StG 715732"],"award-info":[{"award-number":["ERC StG 715732"]}],"id":[{"id":"10.13039\/100010663","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2020,9,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Aims<\/jats:title>\n                  <jats:p>Peripartum cardiomyopathy (PPCM) is a life-threatening heart disease occurring in previously heart-healthy women. A common pathomechanism in PPCM involves the angiostatic 16\u2009kDa-prolactin (16\u2009kDa-PRL) fragment, which via NF-\u03baB-mediated up-regulation of microRNA-(miR)-146a induces vascular damage and heart failure. We analyse whether the plasminogen activator inhibitor-1 (PAI-1) is involved in the pathophysiology of PPCM.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods and results<\/jats:title>\n                  <jats:p>In healthy age-matched postpartum women (PP-Ctrl, n\u2009=\u200953, left ventricular ejection fraction, LVEF\u2009&amp;gt;\u200955%), PAI-1 plasma levels were within the normal range (21\u2009\u00b1\u200910\u2009ng\/mL), but significantly elevated (64\u2009\u00b1\u200938\u2009ng\/mL, P\u2009&amp;lt;\u20090.01) in postpartum PPCM patients at baseline (BL, n\u2009=\u200964, mean LVEF: 23\u2009\u00b1\u20098%). At 6-month follow-up (n\u2009=\u200923), PAI-1 levels decreased (36\u2009\u00b1\u200914\u2009ng\/mL, P\u2009&amp;lt;\u20090.01 vs. BL) and LVEF (49\u2009\u00b1\u200911%) improved. Increased N-terminal pro-brain natriuretic peptide and Troponin T did not correlate with PAI-1. C-reactive protein, interleukin (IL)-6 and IL-1\u03b2 did not differ between PPCM patients and PP-Ctrl. MiR-146a was 3.6-fold (P\u2009&amp;lt;\u20090.001) higher in BL-PPCM plasma compared with PP-Ctrl and correlated positively with PAI-1. In BL-PPCM serum, 16\u2009kDa-PRL coprecipitated with PAI-1, which was associated with higher (P\u2009&amp;lt;\u20090.05) uPAR-mediated NF-\u03baB activation in endothelial cells compared with PP-Ctrl serum. Cardiac biopsies and dermal fibroblasts from PPCM patients displayed higher PAI-1 mRNA levels (P\u2009&amp;lt;\u20090.05) than healthy controls. In PPCM mice (due to a cardiomyocyte-specific-knockout for STAT3, CKO), cardiac PAI-1 expression was higher than in postpartum wild-type controls, whereas a systemic PAI-1-knockout in CKO mice accelerated peripartum cardiac fibrosis, inflammation, heart failure, and mortality.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusion<\/jats:title>\n                  <jats:p>In PPCM patients, circulating and cardiac PAI-1 expression are up-regulated. While circulating PAI-1 may add 16\u2009kDa-PRL to induce vascular impairment via the uPAR\/NF-\u03baB\/miR-146a pathway, experimental data suggest that cardiac PAI-1 expression seems to protect the PPCM heart from fibrosis. Thus, measuring circulating PAI-1 and miR-146a, together with an uPAR\/NF-\u03baB-activity assay could be developed into a specific diagnostic marker assay for PPCM, but unrestricted reduction of PAI-1 for therapy may not be advised.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/cvr\/cvz300","type":"journal-article","created":{"date-parts":[[2019,11,7]],"date-time":"2019-11-07T20:10:08Z","timestamp":1573157408000},"page":"1875-1886","source":"Crossref","is-referenced-by-count":39,"title":["In peripartum cardiomyopathy plasminogen activator inhibitor-1 is a potential new biomarker with controversial roles"],"prefix":"10.1093","volume":"116","author":[{"given":"Melanie","family":"Ricke-Hoch","sequence":"first","affiliation":[{"name":"Department of Cardiology and Angiology, Hannover Medical School, Carl-Neuberg Str. 1, 30625 Hannover, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0234-438X","authenticated-orcid":false,"given":"Martijn F","family":"Hoes","sequence":"additional","affiliation":[{"name":"Department of Cardiology, AB31, University Medical Center Groningen, Hanzeplein 1, 9713 GZ Groningen, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tobias J","family":"Pfeffer","sequence":"additional","affiliation":[{"name":"Department of Cardiology and Angiology, Hannover Medical School, Carl-Neuberg Str. 1, 30625 Hannover, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2257-1536","authenticated-orcid":false,"given":"Stella","family":"Schlothauer","sequence":"additional","affiliation":[{"name":"Department of Cardiology and Angiology, Hannover Medical School, Carl-Neuberg Str. 1, 30625 Hannover, 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Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1376-7318","authenticated-orcid":false,"given":"Christine","family":"Falk","sequence":"additional","affiliation":[{"name":"Institute of Transplant Immunology, IFB-Tx, Hannover Medical School, Hannover, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5646-3237","authenticated-orcid":false,"given":"Arash","family":"Haghikia","sequence":"additional","affiliation":[{"name":"Department of Cardiology and Angiology, Hannover Medical School, Carl-Neuberg Str. 1, 30625 Hannover, Germany"},{"name":"Department of Cardiology, Charit\u00e9 Universit\u00e4tsmedizin Berlin, Campus Benjamin Franklin, Berlin, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ofer","family":"Binah","sequence":"additional","affiliation":[{"name":"Department of Physiology, Ruth & Bruce Rappaport Faculty of Medicine, Technion\u2014Israel 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