{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T00:45:59Z","timestamp":1787013959334,"version":"build-2736575974"},"reference-count":60,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2020,2,11]],"date-time":"2020-02-11T00:00:00Z","timestamp":1581379200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100012698","name":"Jack Brockhoff Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100012698","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000925","name":"National Health and Medical Research Council","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000925","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001043","name":"Cass Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100001043","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2020,4]]},"abstract":"<jats:sec>\n                    <jats:title>Background and purpose<\/jats:title>\n                    <jats:p>Arterial stiffness, a characteristic feature of diabetes, increases the risk of cardiovascular complications. Potential mechanisms that promote arterial stiffness in diabetes include oxidative stress, glycation and inflammation. The anti\u2010inflammatory protein annexin\u2010A1 has cardioprotective properties, particularly in the context of ischaemia. However, the role of endogenous annexin\u2010A1 in the vasculature in both normal physiology and pathophysiology remains largely unknown. Hence, this study investigated the role of endogenous annexin\u2010A1 in diabetes\u2010induced remodelling of mouse mesenteric vasculature.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Experimental approach<\/jats:title>\n                    <jats:p>\n                      Insulin\u2010resistance was induced in male mice (\n                      <jats:italic>AnxA1<\/jats:italic>\n                      <jats:sup>+\/+<\/jats:sup>\n                      and\n                      <jats:italic>AnxA1<\/jats:italic>\n                      <jats:sup>\u2010\/\u2010<\/jats:sup>\n                      ) with the combination of streptozotocin (55mg\/kg i.p. x 3 days) with high fat diet (42% energy from fat) or citrate vehicle with normal chow diet (20\u2010weeks). Insulin\u2010deficiency was induced in a separate cohort of mice using a higher total streptozocin dose (55mg\/kg i.p. x 5 days) on chow diet (16\u2010weeks). At study endpoint, mesenteric artery passive mechanics were assessed by pressure myography.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key results<\/jats:title>\n                    <jats:p>\n                      Insulin\u2010resistance induced significant outward remodelling but had no impact on passive stiffness. Interestingly, vascular stiffness was significantly increased in\n                      <jats:italic>AnxA1<\/jats:italic>\n                      <jats:sup>\u2010\/\u2010<\/jats:sup>\n                      mice when subjected to insulin\u2010resistance. In contrast, insulin\u2010deficiency induced outward remodelling and increased volume compliance in mesenteric arteries, regardless of genotype. In addition, the annexin\u2010A1 \/ formyl peptide receptor axis is upregulated in both insulin\u2010resistant and insulin\u2010deficient mice.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion and implications<\/jats:title>\n                    <jats:p>Our study provided the first evidence that endogenous AnxA1 may play an important vasoprotective role in the context of insulin\u2010resistance. AnxA1\u2010based therapies may provide additional benefits over traditional anti\u2010inflammatory strategies for reducing vascular injury in diabetes.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/bph.14927","type":"journal-article","created":{"date-parts":[[2019,11,13]],"date-time":"2019-11-13T21:58:12Z","timestamp":1573682292000},"page":"1677-1691","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":21,"title":["Annexin\u2010A1 deficiency exacerbates pathological remodelling of the mesenteric vasculature in insulin\u2010resistant, but not insulin\u2010deficient, mice"],"prefix":"10.1111","volume":"177","author":[{"given":"Maria","family":"Jelinic","sequence":"first","affiliation":[{"name":"School of BioSciences University of Melbourne  Melbourne VIC Australia"},{"name":"Department of Physiology, Anatomy and Microbiology La Trobe University  Melbourne VIC 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