{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T22:00:01Z","timestamp":1792188001990,"version":"4.4.0"},"reference-count":49,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2026,1,19]],"date-time":"2026-01-19T00:00:00Z","timestamp":1768780800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,1,19]],"date-time":"2026-01-19T00:00:00Z","timestamp":1768780800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100016168","name":"Ludwig Boltzmann Gesellschaft","doi-asserted-by":"publisher","award":["LBG_KFG_22_32"],"award-info":[{"award-number":["LBG_KFG_22_32"]}],"id":[{"id":"10.13039\/501100016168","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Liver International"],"published-print":{"date-parts":[[2026,2]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background &amp;Aims<\/jats:title>\n                    <jats:p>Growth differentiation factor\u201015 (GDF\u201015), a cell stress\u2010induced cytokine, is implicated in liver disease pathophysiology. We investigated GDF\u201015 in cirrhosis, focusing on its association with disease\u2010driving pathomechanisms, platelet function, hepatic decompensation, and mortality.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We included patients with cirrhosis undergoing hepatic venous pressure gradient (HVPG) measurement at the Vienna General Hospital. Platelet surface P\u2010selectin and glycoprotein IIb\/IIIa (GPIIb\/IIIa) expression after agonist stimulation were assessed by flow cytometry as platelet activation markers. GDF\u201015 serum levels were quantified by electrochemiluminescence immunoassay.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Among 106 patients (median age 55.1\u2009years; 70.8% male), median GDF\u201015 was 2880 (1850\u20134770)\u2009pg\/mL. GDF\u201015 correlated with hepatic dysfunction (MELD Spearman's\n                      <jats:italic>\u03c1<\/jats:italic>\n                      : 0.50; albumin\n                      <jats:italic>\u03c1<\/jats:italic>\n                      : \u22120.57), HVPG (\n                      <jats:italic>\u03c1<\/jats:italic>\n                      : 0.47), systemic inflammation (C\u2010reactive protein\n                      <jats:italic>\u03c1<\/jats:italic>\n                      : 0.45; interleukin 6 [IL\u20106]\n                      <jats:italic>\u03c1<\/jats:italic>\n                      : 0.55; procalcitonin\n                      <jats:italic>\u03c1<\/jats:italic>\n                      : 0.58), liver stiffness (\n                      <jats:italic>\u03c1<\/jats:italic>\n                      : 0.67) and enhanced liver fibrosis test (\n                      <jats:italic>\u03c1<\/jats:italic>\n                      : 0.64) (all\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001). GDF\u201015 was higher in patients with detectable bacterial DNA in blood (3520 vs. 2250\u2009pg\/mL;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001) and correlated with lipopolysaccharide (\n                      <jats:italic>\u03c1<\/jats:italic>\n                      : 0.34;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.010) and lipoteichoic acid (\n                      <jats:italic>\u03c1<\/jats:italic>\n                      : 0.37;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.004). Platelet activation was not linked to GDF\u201015 after adjusting for liver disease severity, yet patients with undetectable GPIIb\/IIIa activation after stimulation showed significantly higher GDF\u201015. Over a median follow\u2010up of 51.5 (26.0\u201358.2) months, 38 patients decompensated and 21 died (61.9% liver\u2010related). GDF\u201015 (aHR per 100 pg\/mL: 1.015; 95% CI: 1.004\u20131.026;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.007) predicted decompensation risk independently of HVPG, MELD, albumin and IL\u20106. Similarly, GDF\u201015 was associated with higher risk of all\u2010cause (HR: 1.019; 95% CI: 1.009\u20131.029;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001) and liver\u2010related mortality (HR: 1.019; 95% CI: 1.007\u20131.032;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.002).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>GDF\u201015 is a promising biomarker in cirrhosis that reflects disease\u2010driving pathomechanisms and independently predicts decompensation and mortality.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/liv.70516","type":"journal-article","created":{"date-parts":[[2026,1,20]],"date-time":"2026-01-20T06:45:37Z","timestamp":1768891537000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["<scp>GDF<\/scp>\n                    \u201015 Levels in Cirrhosis Are Linked to Hepatic Fibrogenesis, Bacterial Translocation, and Worse Clinical Outcomes"],"prefix":"10.1111","volume":"46","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3403-3372","authenticated-orcid":false,"given":"Benedikt Silvester","family":"Hofer","sequence":"first","affiliation":[{"name":"Division of Gastroenterology and Hepatology, Department of Medicine III Medical University of Vienna  Vienna Austria"},{"name":"Division of Gastroenterology and Hepatology, Department of Medicine III, Vienna Hepatic Hemodynamic Laboratory Medical University of Vienna  Vienna Austria"},{"name":"Christian Doppler Lab for Portal Hypertension and 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II Medical University of Vienna  Vienna Austria"},{"name":"Institute of Cardiovascular Pharmacotherapy and Interventional Cardiology, Karl Landsteiner Society  St. P\u00f6lten Austria"},{"name":"Department of Internal Medicine I Cardiology and Intensive Care Medicine, Landesklinikum Mistelbach\u2010G\u00e4nserndorf  Mistelbach Austria"},{"name":"Karl Landsteiner University of Health Sciences  Krems 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