{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T12:04:47Z","timestamp":1792065887319,"version":"4.4.0"},"reference-count":43,"publisher":"American Diabetes Association","issue":"12","license":[{"start":{"date-parts":[[2018,11,20]],"date-time":"2018-11-20T00:00:00Z","timestamp":1542672000000},"content-version":"vor","delay-in-days":68,"URL":"http:\/\/www.diabetesjournals.org\/content\/license"}],"funder":[{"DOI":"10.13039\/501100002081","name":"Irish Research Council","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100002081","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100010665","name":"H2020 Marie Sk\u0142odowska-Curie Actions","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100010665","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000925","name":"NHMRC","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000925","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001067","name":"JDRF Australia","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100001067","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2018,12,1]]},"abstract":"<jats:p>Increasing evidence points to the fact that defects in the resolution of inflammatory pathways predisposes individuals to the development of chronic inflammatory diseases, including diabetic complications such as accelerated atherosclerosis. The resolution of inflammation is dynamically regulated by the production of endogenous modulators of inflammation, including lipoxin A4 (LXA4). Here, we explored the therapeutic potential of LXA4 and a synthetic LX analog (Benzo-LXA4) to modulate diabetic complications in the streptozotocin-induced diabetic ApoE\u2212\/\u2212 mouse and in human carotid plaque tissue ex vivo. The development of diabetes-induced aortic plaques and inflammatory responses of aortic tissue, including the expression of vcam-1, mcp-1, il-6, and il-1\u03b2, was significantly attenuated by both LXA4 and Benzo-LXA4 in diabetic ApoE\u2212\/\u2212 mice. Importantly, in mice with established atherosclerosis, treatment with LXs for a 6-week period, initiated 10 weeks after diabetes onset, led to a significant reduction in aortic arch plaque development (19.22 \u00b1 2.01% [diabetic]; 12.67 \u00b1 1.68% [diabetic + LXA4]; 13.19 \u00b1 1.97% [diabetic + Benzo-LXA4]). Secretome profiling of human carotid plaque explants treated with LXs indicated changes to proinflammatory cytokine release, including tumor necrosis factor-\u03b1 and interleukin-1\u03b2. LXs also inhibited platelet-derived growth factor\u2013stimulated vascular smooth muscle cell proliferation and transmigration and endothelial cell inflammation. These data suggest that LXs may have therapeutic potential in the context of diabetes-associated vascular complications.<\/jats:p>","DOI":"10.2337\/db17-1317","type":"journal-article","created":{"date-parts":[[2018,9,13]],"date-time":"2018-09-13T12:15:16Z","timestamp":1536840916000},"page":"2657-2667","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":85,"title":["Lipoxins Protect Against Inflammation in Diabetes-Associated Atherosclerosis"],"prefix":"10.2337","volume":"67","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4908-5474","authenticated-orcid":false,"given":"Eoin P.","family":"Brennan","sequence":"first","affiliation":[{"name":"UCD Diabetes Complications Research Centre, UCD Conway Institute of Biomolecular and Biomedical Research, UCD School of Medicine, University College Dublin, Dublin, Ireland"},{"name":"JDRF Danielle Alberti Memorial Centre for Diabetes Complications, Diabetes Division, Baker Heart and 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