{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,6]],"date-time":"2026-11-06T17:26:08Z","timestamp":1793985968188,"version":"4.8.0"},"reference-count":36,"publisher":"Oxford University Press (OUP)","issue":"15","license":[{"start":{"date-parts":[[2026,9,7]],"date-time":"2026-09-07T00:00:00Z","timestamp":1788739200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"British Heart Foundation Senior Basic Science Research Fellowships","award":["FS\/13\/48\/30453"],"award-info":[{"award-number":["FS\/13\/48\/30453"]}],"id":[{"id":"https:\/\/ror.org\/02wdwnk04","id-type":"ROR","asserted-by":"crossref"}]},{"name":"British Heart Foundation Senior Basic Science Research Fellowships","award":["FS\/18\/52\/33808"],"award-info":[{"award-number":["FS\/18\/52\/33808"]}],"id":[{"id":"https:\/\/ror.org\/02wdwnk04","id-type":"ROR","asserted-by":"crossref"}]},{"name":"British Heart Foundation Intermediate Clinical Fellowship","award":["FS\/18\/13\/33281"],"award-info":[{"award-number":["FS\/18\/13\/33281"]}],"id":[{"id":"https:\/\/ror.org\/02wdwnk04","id-type":"ROR","asserted-by":"crossref"}]},{"name":"British Heart Foundation Imperial Centre of Research Excellence Award","award":["RE\/18\/4\/34215"],"award-info":[{"award-number":["RE\/18\/4\/34215"]}],"id":[{"id":"https:\/\/ror.org\/02wdwnk04","id-type":"ROR","asserted-by":"crossref"}]},{"name":"British Heart Foundation Imperial Centre of Research Excellence Award","award":["RE\/24\/130023"],"award-info":[{"award-number":["RE\/24\/130023"]}],"id":[{"id":"https:\/\/ror.org\/02wdwnk04","id-type":"ROR","asserted-by":"crossref"}]},{"DOI":"10.13039\/501100013342","name":"NIHR Imperial Biomedical Research Centre","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100013342","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","award":["268555672-SFB1213"],"award-info":[{"award-number":["268555672-SFB1213"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,11,6]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aims<\/jats:title>\n                    <jats:p>Pulmonary arterial hypertension (PAH) is driven by sustained vasoconstriction and structural remodelling of distal pulmonary arteries. We have previously demonstrated that osteoprotegerin (OPG, tnfrsf11b) is upregulated in PAH animal models and patient tissues, with circulating levels being prognostic. OPG knock-out (KO) mice exhibit an attenuated PAH phenotype, and therapeutic inhibition using a human monoclonal anti-OPG antibody reduces disease severity in multiple rodent models. However, the key cellular source of pathogenic OPG and the mechanism underlying therapeutic blockade remain unknown.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and results<\/jats:title>\n                    <jats:p>To define the main cellular source of OPG, conditional Tnfrsf11b deletion was generated by crossing OPGfl\/fl mice with PGKcretg\/+ (global), LysMcretg\/+ (myeloid), Myl2cretg\/+ (cardiac myocytes), Cdh5cretg\/+ (endothelial cells), smMHCcretg\/+ [vascular smooth muscle cell (VSMCs)], Col1a2cretg\/+ (fibroblasts). KOs were induced by tamoxifen injection, and PAH established using Sugen5416\/hypoxia (SuHx) model. Cardiopulmonary phenotyping included echocardiography, cardiac catheterization, and histological analysis. Mechanistic studies were performed in VSMCs using peptide-based kinase activity profiling (PamStation).<\/jats:p>\n                    <jats:p>PGKcretg\/+\/OPGfl\/fl mice phenocopied the previous results obtained with global OPG KO (OPG\u2212\/\u2212). Only VSMC-specific deletion (smMHCcretg\/0\/OPGfl\/fl) resulted in significantly improved haemodynamic parameters, evidenced by reduced right ventricular systolic pressure and pulmonary vascular resistance, and reduced pulmonary vascular remodelling demonstrating that VSMC-derived OPG is the primary driver of PAH pathogenesis.<\/jats:p>\n                    <jats:p>Kinome profiling of control and idiopathic PAH (IPAH)-pulmonary artery smooth muscle cells (PASMCs) treated with OPG+\/\u2212 anti-OPG antibody revealed IPAH-specific regulation of PI3K\u2013Akt and enrichment of pathways involving autophagy, and longevity regulation linked to cellular stress resistance and growth. Anti-OPG antibody treatment reduced AKT phosphorylation in IPAH-PASMCs. Knock-down of AKT1 by siRNA reduced OPG-induced proliferation and migration of human PASMCs. These results align with emerging data implicating OPG in cellular senescence and vascular ageing.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Together, these findings highlight VSMC-derived OPG as a critical mediator of pulmonary vascular remodelling in PAH pathogenesis and suggest that targeting OPG via a therapeutic antibody is mediated through PI3K\u2013Akt signalling.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/cvr\/cvag197","type":"journal-article","created":{"date-parts":[[2026,9,4]],"date-time":"2026-09-04T11:29:29Z","timestamp":1788521369000},"page":"2189-2203","source":"Crossref","is-referenced-by-count":0,"title":["Vascular smooth muscle cell-derived osteoprotegerin drives pulmonary arterial hypertension via AKT activation and is attenuated by monoclonal antibody 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(DZL), Excellence Cluster Cardio-Pulmonary Institute (CPI), Institute for Lung Health (ILH), Justus Liebig University , Giessen ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nadiya V","family":"Mykytyuk","sequence":"additional","affiliation":[{"name":"National Heart and Lung Institute, Faculty of Medicine, Imperial College London , London W12 0NN ,","place":["UK"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julia","family":"Baldauf","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, German Center for Lung Research (DZL), Excellence Cluster Cardio-Pulmonary Institute (CPI), Institute for Lung Health (ILH), Justus Liebig University , Giessen ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Josephine A","family":"Pickworth","sequence":"additional","affiliation":[{"name":", University of Sheffield School of Medicine and Population Health , Sheffield ,","place":["UK"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amira A","family":"Zawia","sequence":"additional","affiliation":[{"name":", University of Sheffield School of Medicine and Population Health , Sheffield ,","place":["UK"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Helena A","family":"Turton","sequence":"additional","affiliation":[{"name":", University of Sheffield School of Medicine and Population Health , Sheffield ,","place":["UK"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Megan F","family":"Allen","sequence":"additional","affiliation":[{"name":", University of Sheffield School of Medicine and Population Health , Sheffield ,","place":["UK"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0938-2469","authenticated-orcid":false,"given":"Clemens","family":"Ruppert","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, German Center for Lung 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