{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T19:25:35Z","timestamp":1790623535369,"version":"4.1.0"},"reference-count":46,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[2021,1,23]],"date-time":"2021-01-23T00:00:00Z","timestamp":1611360000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"name":"Swiss National Research Foundation","award":["Nr.S-85708-03-01"],"award-info":[{"award-number":["Nr.S-85708-03-01"]}]},{"name":"Swiss National Research Foundation","award":["Nr.310030_175546"],"award-info":[{"award-number":["Nr.310030_175546"]}]},{"name":"Swiss National Research Foundation","award":["31030_166576"],"award-info":[{"award-number":["31030_166576"]}]},{"DOI":"10.13039\/501100004362","name":"Swiss Heart Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100004362","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Alfred and Annemarie von Sick Grants for Translational and Clinical Research Cardiology and Oncology"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2022,1,7]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Aims<\/jats:title>\n                  <jats:p>Rheumatoid arthritis (RA) is a chronic inflammatory disease affecting joints and blood vessels. Despite low levels of low-density lipoprotein cholesterol (LDL-C), RA patients exhibit endothelial dysfunction and are at increased risk of death from cardiovascular complications, but the molecular mechanism of action is unknown. We aimed in the present study to identify the molecular mechanism of endothelial dysfunction in a mouse model of RA and in patients with RA.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods and results<\/jats:title>\n                  <jats:p>Endothelium-dependent relaxations to acetylcholine were reduced in aortae of two tumour necrosis factor alpha (TNF\u03b1) transgenic mouse lines with either mild (Tg3647) or severe (Tg197) forms of RA in a time- and severity-dependent fashion as assessed by organ chamber myograph. In Tg197, TNF\u03b1 plasma levels were associated with severe endothelial dysfunction. LOX-1 receptor was markedly up-regulated leading to increased vascular oxLDL uptake and NF\u03baB-mediated enhanced Arg2 expression via direct binding to its promoter resulting in reduced NO bioavailability and vascular cGMP levels as shown by ELISA and chromatin immunoprecipitation. Anti-TNF\u03b1 treatment with infliximab normalized endothelial function together with LOX-1 and Arg2 serum levels in mice. In RA patients, soluble LOX-1 serum levels were also markedly increased and closely related to serum levels of C-reactive protein. Similarly, ARG2 serum levels were increased. Similarly, anti-TNF\u03b1 treatment restored LOX-1 and ARG2 serum levels in RA patients.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>Increased TNF\u03b1 levels not only contribute to RA, but also to endothelial dysfunction by increasing vascular oxLDL content and activation of the LOX-1\/NF\u03baB\/Arg2 pathway leading to reduced NO bioavailability and decreased cGMP levels. Anti-TNF\u03b1 treatment improved both articular symptoms and endothelial function by reducing LOX-1, vascular oxLDL, and Arg2 levels.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/cvr\/cvab005","type":"journal-article","created":{"date-parts":[[2021,1,9]],"date-time":"2021-01-09T13:51:32Z","timestamp":1610200292000},"page":"254-266","source":"Crossref","is-referenced-by-count":32,"title":["TNF\u03b1 induces endothelial dysfunction in rheumatoid arthritis via LOX-1 and arginase 2: reversal by monoclonal TNF\u03b1 antibodies"],"prefix":"10.1093","volume":"118","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3052-9493","authenticated-orcid":false,"given":"Alexander","family":"Akhmedov","sequence":"first","affiliation":[{"name":"Center for Molecular Cardiology, Schlieren Campus, University of Zurich, 8001 Zurich, Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Margot","family":"Crucet","sequence":"additional","affiliation":[{"name":"Center for 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