{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,8]],"date-time":"2026-09-08T11:29:28Z","timestamp":1788866968986,"version":"build-2803163510"},"reference-count":47,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2021,4,29]],"date-time":"2021-04-29T00:00:00Z","timestamp":1619654400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"DOI":"10.13039\/100000968","name":"American Heart Association [AHA","doi-asserted-by":"crossref","award":["TPA34860015"],"award-info":[{"award-number":["TPA34860015"]}],"id":[{"id":"10.13039\/100000968","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["HL121531"],"award-info":[{"award-number":["HL121531"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["HL14715"],"award-info":[{"award-number":["HL14715"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["T32HL007101"],"award-info":[{"award-number":["T32HL007101"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Edna and Fred L. Mandel Jr Foundation"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2022,2,21]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aims\u2003<\/jats:title>\n                    <jats:p>The F-actin-binding protein Drebrin inhibits smooth muscle cell (SMC) migration, proliferation, and pro-inflammatory signalling. Therefore, we tested the hypothesis that Drebrin constrains atherosclerosis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and results<\/jats:title>\n                    <jats:p>SM22-Cre+\/Dbnflox\/flox\/Ldlr\u2212\/\u2212 (SMC-Dbn\u2212\/\u2212\/Ldlr\u2212\/\u2212) and control mice (SM22-Cre+\/Ldlr\u2212\/\u2212, Dbnflox\/flox\/Ldlr\u2212\/\u2212, and Ldlr\u2212\/\u2212) were fed a western diet for 14\u201320\u2009weeks. Brachiocephalic arteries of SMC-Dbn \u2212\/\u2212\/Ldlr\u2212\/\u2212 mice exhibited 1.5- or 1.8-fold greater cross-sectional lesion area than control mice at 14 or 20 weeks, respectively. Aortic atherosclerotic lesion surface area was 1.2-fold greater in SMC-Dbn\u2212\/\u2212\/Ldlr\u2212\/\u2212 mice. SMC-Dbn\u2212\/\u2212\/Ldlr\u2212\/\u2212 lesions comprised necrotic cores that were two-fold greater in size than those of control mice. Consistent with their bigger necrotic core size, lesions in SMC-Dbn\u2212\/\u2212 arteries also showed more transdifferentiation of SMCs to macrophage-like cells: 1.5- to 2.5-fold greater, assessed with BODIPY or with CD68, respectively. In vitro data were concordant: Dbn\u2212\/\u2212 SMCs had 1.7-fold higher levels of KLF4 and transdifferentiated to macrophage-like cells more readily than Dbnflox\/flox SMCs upon cholesterol loading, as evidenced by greater up-regulation of CD68 and galectin-3. Adenovirally mediated Drebrin rescue produced equivalent levels of macrophage-like transdifferentiation in Dbn\u2212\/\u2212 and Dbnflox\/flox SMCs. During early atherogenesis, SMC-Dbn\u2212\/\u2212\/Ldlr\u2212\/\u2212 aortas demonstrated 1.6-fold higher levels of reactive oxygen species than control mouse aortas. The 1.8-fold higher levels of Nox1 in Dbn\u2212\/\u2212 SMCs were reduced to WT levels with KLF4 silencing. Inhibition of Nox1 chemically or with siRNA produced equivalent levels of macrophage-like transdifferentiation in Dbn\u2212\/\u2212 and Dbnflox\/flox SMCs.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion\u2003<\/jats:title>\n                    <jats:p>We conclude that SMC Drebrin limits atherosclerosis by constraining SMC Nox1 activity and SMC transdifferentiation to macrophage-like cells.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/cvr\/cvab156","type":"journal-article","created":{"date-parts":[[2021,4,27]],"date-time":"2021-04-27T15:32:29Z","timestamp":1619537549000},"page":"772-784","source":"Crossref","is-referenced-by-count":23,"title":["Drebrin attenuates atherosclerosis by limiting smooth muscle cell transdifferentiation"],"prefix":"10.1093","volume":"118","author":[{"given":"Jiao-Hui","family":"Wu","sequence":"first","affiliation":[{"name":"Department of Medicine (Cardiology), Duke University 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27710, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elizabeth R","family":"Hauser","sequence":"additional","affiliation":[{"name":"Department of Biostatistics & Bioinformatics, Duke University School of Medicine, Durham, NC 27710, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5822-0549","authenticated-orcid":false,"suffix":"Jr","given":"Francis J","family":"Miller","sequence":"additional","affiliation":[{"name":"Department of Medicine, Wake Forest Baptist Medical Center, Winston-Salem, NC 27157, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Neil J","family":"Freedman","sequence":"additional","affiliation":[{"name":"Department of Medicine (Cardiology), Duke University Medical Center, 10 Duke Medicine Circle, Durham, NC 27710, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2301-585X","authenticated-orcid":false,"given":"Jonathan 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