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We hypothesized that the liver promotes inflammatory injury to the pulmonary endothelium. PAH patients without liver disease with pulmonary artery endothelial cell (PAEC) biopsies were included. Unsupervised CART analysis of liver serologies identified subclinical dysfunction clusters; machine\u2010learning models informed differential expression and protein\u2013protein interaction network assembly. PAEC transcriptomes were compared to liver and lung data from monocrotaline and Sugen\u2010Hypoxia rats. Liver fibrosis was assessed in rat and human PAH livers. Among 25 PAH patients (76% female, median age 61 [30\u201384] years), CART identified clusters distinguished by Model for End\u2010Stage Liver Disease Sodium (MELD\u2010Na) \u2265\u200912, which was associated with higher Fibrosis\u20104 scores and higher pulmonary vascular resistance (\u00df\u2009=\u20090.5 Wood units per point increase in MELD\u2010Na, 95% CI 0.2\u20130.8,\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.005) after adjustment for right atrial pressure. Subjects with MELD\u2010Na \u2265\u200912 had decreased 6\u2010min walk distance (353 [120\u2013576] m vs. 411 [300\u2013600] m,\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.03). In comparing the two clusters, a protein\u2013protein interaction network analysis identified IL\u20106 as the primary hub of a transcriptional module enriched for leukocyte chemotaxis and myeloid leukocyte migration (all FDR &lt;\u20090.05) among the High\u2010MELD\u2010Na group. Rat livers demonstrated immune activation and a trend toward increased fibrosis (20.8 vs. 16.6% area stained,\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.09), and human PAH livers without liver disease showed an intermediate fibrotic phenotype between controls and portopulmonary hypertension, though this did not reach statistical significance. Our observations support a lung\u2013liver axis in PAH even in the absence of liver disease, warranting further study.\n                  <\/jats:p>","DOI":"10.1002\/cph4.70171","type":"journal-article","created":{"date-parts":[[2026,5,15]],"date-time":"2026-05-15T14:02:26Z","timestamp":1778853746000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Exploring the Lung\u2013Liver Axis in Pulmonary Arterial Hypertension"],"prefix":"10.1002","volume":"16","author":[{"given":"Navneet","family":"Singh","sequence":"first","affiliation":[{"name":"Department of Medicine The Warren Alpert School of Medicine at Brown University  Providence Rhode Island USA"},{"name":"Center for Advanced Lung Care Brown University Health  Providence Rhode Island USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jordan","family":"Lawson","sequence":"additional","affiliation":[{"name":"COBRE Center for Computational Biology of 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