{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,19]],"date-time":"2026-10-19T03:39:43Z","timestamp":1792381183980,"version":"4.4.0"},"reference-count":46,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T00:00:00Z","timestamp":1792108800000},"content-version":"vor","delay-in-days":15,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T00:00:00Z","timestamp":1790812800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Clin Exp Pharma Physio"],"published-print":{"date-parts":[[2026,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Pulmonary arterial hypertension (PAH) is characterized by pulmonary endothelial cell (EC) dysfunction and pulmonary vascular remodelling. Endothelial\u2010to\u2010mesenchymal transition (EndMT) is a key mechanism underlying pulmonary vascular remodelling. Krev interaction trapped protein 1 (KRIT1) plays a crucial role in maintaining vascular endothelial stability, but its association with PAH remains unclear. Analysis of RNA expression microarray data from the GEO database revealed that KRIT1 expression was downregulated in the lung tissues of PAH patients. In the monocrotaline (MCT)\u2010induced PAH rat model, KRIT1 expression in lung tissue was reduced, accompanied by typical PAH phenotypes, including elevated right ventricular systolic pressure, right ventricular hypertrophy, and increased pulmonary artery wall thickness. In\u00a0vitro, EndMT in primary rat pulmonary artery ECs (rPAECs) was induced by inflammatory cytokines, and KRIT1 expression was suppressed during this process. Overexpression of KRIT1 attenuated the EndMT\u2010associated molecular phenotype, with increased VE\u2010cadherin and reduced \u03b1\u2010SMA expression, and inhibited the enhanced migratory activity of rPAECs. Mechanistically, KRIT1 may exert anti\u2010EndMT effects by negatively regulating the TGF\u2010\u03b2\/Smad signalling pathway, as evidenced by reduced Smad2\/3 phosphorylation. This effect was abrogated by a TGF\u2010\u03b2\/Smad pathway agonist. In addition, KRIT1 overexpression suppressed \u03b2\u2010catenin nuclear translocation. This study reveals a role for KRIT1 in maintaining endothelial homeostasis, suggesting its potential involvement in PAH\u2010associated vascular remodelling.<\/jats:p>","DOI":"10.1111\/1440-1681.70161","type":"journal-article","created":{"date-parts":[[2026,10,17]],"date-time":"2026-10-17T05:16:28Z","timestamp":1792214188000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["<scp>KRIT1<\/scp>\n                    Inhibits\n                    <scp>TGF<\/scp>\n                    \u2010\u03b2\/Smad\u2010Mediated Endothelial\u2010To\u2010Mesenchymal Transition in Pulmonary Arterial Hypertension"],"prefix":"10.1111","volume":"53","author":[{"ORCID":"https:\/\/orcid.org\/0009-0001-2642-8764","authenticated-orcid":false,"given":"Debin","family":"Ma","sequence":"first","affiliation":[{"name":"Department of Respiratory and Critical Care Medicine General Hospital of Northern Theater Command  Shenyang 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