{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T23:29:32Z","timestamp":1777937372828,"version":"3.51.4"},"reference-count":44,"publisher":"SAGE Publications","issue":"10","license":[{"start":{"date-parts":[[2019,7,9]],"date-time":"2019-07-09T00:00:00Z","timestamp":1562630400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"funder":[{"DOI":"10.13039\/501100024075","name":"Region of Southern Denmark","doi-asserted-by":"crossref","id":[{"id":"10.13039\/501100024075","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100008361","name":"Scleroseforeningen","doi-asserted-by":"publisher","award":["A29829"],"award-info":[{"award-number":["A29829"]}],"id":[{"id":"10.13039\/100008361","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100008361","name":"Scleroseforeningen","doi-asserted-by":"publisher","award":["A32766"],"award-info":[{"award-number":["A32766"]}],"id":[{"id":"10.13039\/100008361","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100008361","name":"Scleroseforeningen","doi-asserted-by":"publisher","award":["A34367"],"award-info":[{"award-number":["A34367"]}],"id":[{"id":"10.13039\/100008361","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100004836","name":"Det Frie Forskningsrd","doi-asserted-by":"publisher","award":["DFF-1333-00111"],"award-info":[{"award-number":["DFF-1333-00111"]}],"id":[{"id":"10.13039\/501100004836","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100004836","name":"Det Frie Forskningsrd","doi-asserted-by":"publisher","award":["DFF-6110-00636"],"award-info":[{"award-number":["DFF-6110-00636"]}],"id":[{"id":"10.13039\/501100004836","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Slagelse Hospital Research Fund"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Mult Scler"],"published-print":{"date-parts":[[2020,9]]},"abstract":"<jats:sec>\n                    <jats:title>Background:<\/jats:title>\n                    <jats:p>Neuromyelitis optica spectrum disorder (NMOSD) is a relapsing inflammatory central nervous system (CNS) disease for which there is no cure. Immunoglobulin G autoantibodies specific for the water channel aquaporin-4 are a serum biomarker, believed to induce complement-dependent astrocyte damage with secondary demyelination.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective:<\/jats:title>\n                    <jats:p>To investigate the effect of angiotensin AT2 receptor (AT2R) stimulation on NMOSD-like pathology and its underlying mechanism.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>NMOSD-like pathology was induced in mice by intracerebral injection of immunoglobulin-G isolated from NMOSD patient serum, with complement. This mouse model produces the characteristic histological features of NMOSD. A specific AT2R agonist, Compound 21 (C21), was given intracerebrally at day 0 and by intrathecal injection at day 2.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>Loss of aquaporin-4 and glial fibrillary acidic protein was attenuated by treatment with C21. Administration of C21 induced mRNA for interleukin-10 in the brain. NMOSD-like pathology was exacerbated in interleukin-10-deficient mice, suggesting a protective role. C21 treatment did not attenuate NMOSD-like pathology in interleukin-10-deficient mice, indicating that the protective effect of AT2R stimulation was dependent on interleukin-10.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion:<\/jats:title>\n                    <jats:p>Our findings identify AT2R as a novel potential therapeutic target for the treatment of NMOSD. Interleukin-10 signaling is an essential part of the protective mechanism counteracting NMOSD pathology.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/1352458519860327","type":"journal-article","created":{"date-parts":[[2019,7,9]],"date-time":"2019-07-09T10:16:22Z","timestamp":1562667382000},"page":"1187-1196","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":9,"title":["Angiotensin AT2 receptor\u2013induced interleukin-10 attenuates neuromyelitis optica spectrum disorder\u2013like pathology"],"prefix":"10.1177","volume":"26","author":[{"given":"Reza","family":"Khorooshi","sequence":"first","affiliation":[{"name":"Department of Neurobiology Research, Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Emil Ulrikkaholm","family":"Tofte-Hansen","sequence":"additional","affiliation":[{"name":"Department of 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