{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T22:44:10Z","timestamp":1790289850544,"version":"4.1.0"},"reference-count":70,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2019,8,11]],"date-time":"2019-08-11T00:00:00Z","timestamp":1565481600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2019,8,11]],"date-time":"2019-08-11T00:00:00Z","timestamp":1565481600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["1R01AR066629- 01A1"],"award-info":[{"award-number":["1R01AR066629- 01A1"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2019,10]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Marfan syndrome (MFS) is a connective tissue disorder that results in aortic root aneurysm formation. Reactive oxygen species (ROS) seem to play a role in aortic wall remodelling in MFS, although the mechanism remains unknown. MFS\n                    <jats:italic>\n                      Fbn1\n                      <jats:sup>C1039G\/+<\/jats:sup>\n                    <\/jats:italic>\n                    mouse root\/ascending (AS) and descending (DES) aortic samples were examined using DHE staining, lucigenin\u2010enhanced chemiluminescence (LGCL), Verhoeff's elastin\u2010Van Gieson staining (elastin breakdown) and in situ zymography for protease activity.\n                    <jats:italic>\n                      Fbn1\n                      <jats:sup>C1039G\/+<\/jats:sup>\n                    <\/jats:italic>\n                    AS\u2010 or DES\u2010derived smooth muscle cells (SMC) were treated with anti\u2010TGF\u2010\u03b2 antibody, angiotensin II (AngII), anti\u2010TGF\u2010\u03b2 antibody\u00a0+\u00a0AngII, or isotype control. ROS were detected during early aneurysm formation in the\n                    <jats:italic>\n                      Fbn1\n                      <jats:sup>C1039G\/+<\/jats:sup>\n                    <\/jats:italic>\n                    AS aorta, but absent in normal\u2010sized DES aorta.\n                    <jats:italic>\n                      Fbn1\n                      <jats:sup>C1039G\/+<\/jats:sup>\n                    <\/jats:italic>\n                    mice treated with the unspecific NADPH oxidase inhibitor, apocynin reduced AS aneurysm formation, with attenuated elastin fragmentation. In situ zymography revealed apocynin treatment decreased protease activity. In vitro SMC studies showed\n                    <jats:italic>\n                      Fbn1\n                      <jats:sup>C1039G\/+<\/jats:sup>\n                    <\/jats:italic>\n                    \u2010derived AS SMC had increased NADPH activity compared to DES\u2010derived SMC. AS SMC NADPH activity increased with AngII treatment and appeared TGF\u2010\u03b2 dependent. In conclusion, ROS play a role in MFS aneurysm development and correspond anatomically with aneurysmal aortic segments. ROS inhibition via apocynin treatment attenuates MFS aneurysm progression. AngII enhances ROS production in MFS AS SMCs and is likely TGF\u2010\u03b2 dependent.\n                  <\/jats:p>","DOI":"10.1111\/jcmm.14587","type":"journal-article","created":{"date-parts":[[2019,8,12]],"date-time":"2019-08-12T00:04:20Z","timestamp":1565568260000},"page":"7000-7009","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":30,"title":["Anatomically specific reactive oxygen species production participates in Marfan syndrome aneurysm formation"],"prefix":"10.1111","volume":"23","author":[{"given":"Fabian","family":"Emrich","sequence":"first","affiliation":[{"name":"Department of Cardiothoracic Surgery Stanford University Stanford California"},{"name":"Department of Cardiothoracic Surgery Leipzig University Heart Center Leipzig Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kiril","family":"Penov","sequence":"additional","affiliation":[{"name":"Department of Cardiothoracic Surgery Stanford 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