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Annexin A1 (ANXA1) is an endogenous anti-inflammatory molecule that limits and resolves inflammation. In this study, we have used a bedside to bench approach to investigate: (1) ANXA1 levels in individuals with type 1 diabetes; (2) the role of endogenous ANXA1 in nephropathy and cardiomyopathy in experimental type 1 diabetes; and (3) whether treatment with human recombinant ANXA1 attenuates nephropathy and cardiomyopathy in a murine model of type 1 diabetes.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Methods<\/jats:title>\n            <jats:p>ANXA1 was measured in plasma from individuals with type 1 diabetes with or without nephropathy and healthy donors. Experimental type 1 diabetes was induced in mice by injection of streptozotocin (STZ; 45\u00a0mg\/kg i.v. per day for 5 consecutive days) in C57BL\/6 or <jats:italic>Anxa1<\/jats:italic>\n              <jats:sup>\u2212\/\u2212<\/jats:sup> mice. Diabetic mice were treated with human recombinant (hr)ANXA1 (1\u00a0\u03bcg, 100\u00a0\u03bcl, 50\u00a0mmol\/l HEPES; 140\u00a0mmol\/l NaCl; pH\u00a07.4, i.p.) or vehicle (100\u00a0\u03bcl, 50\u00a0mmol\/l HEPES; 140\u00a0mmol\/l NaCl; pH\u00a07.4, i.p.).<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results<\/jats:title>\n            <jats:p>Plasma levels of ANXA1 were elevated in individuals with type 1 diabetes with\/without nephropathy compared with healthy individuals (66.0\u00a0\u00b1\u00a04.2\/64.0\u00a0\u00b1\u00a04\u00a0ng\/ml vs 35.9\u00a0\u00b1\u00a02.3\u00a0ng\/ml; <jats:italic>p<\/jats:italic>\u00a0&lt;\u00a00.05). Compared with diabetic wild-type (WT) mice, diabetic <jats:italic>Anxa1<\/jats:italic>\n              <jats:sup>\u2212\/\u2212<\/jats:sup> mice exhibited a worse diabetic phenotype and developed more severe cardiac (ejection fraction; 76.1\u00a0\u00b1\u00a01.6% vs 49.9\u00a0\u00b1\u00a00.9%) and renal dysfunction (proteinuria; 89.3\u00a0\u00b1\u00a05.0\u00a0\u03bcg\/mg vs 113.3\u00a0\u00b1\u00a05.5\u00a0\u03bcg\/mg). Mechanistically, compared with non-diabetic WT mice, the degree of the phosphorylation of mitogen-activated protein kinases (MAPKs) p38, c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) was significantly higher in non-diabetic <jats:italic>Anxa1<\/jats:italic>\n              <jats:sup>\u2212\/\u2212<\/jats:sup> mice in both the heart and kidney, and was further enhanced after STZ-induced type 1 diabetes. Prophylactic treatment with hrANXA1 (weeks 1\u201313) attenuated both cardiac (ejection fraction; 54.0\u00a0\u00b1\u00a01.6% vs 72.4\u00a0\u00b1\u00a01.0%) and renal (proteinuria; 89.3\u00a0\u00b1\u00a05.0\u00a0\u03bcg\/mg vs 53.1\u00a0\u00b1\u00a03.4\u00a0\u03bcg\/mg) dysfunction associated with STZ-induced diabetes, while therapeutic administration of hrANXA1 (weeks 8\u201313), after significant cardiac and renal dysfunction had already developed, halted the further functional decline in cardiac and renal function seen in diabetic mice administered vehicle. In addition, administration of hrANXA1 attenuated the increase in phosphorylation of p38, JNK and ERK, and restored phosphorylation of Akt in diabetic mice.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions\/interpretation<\/jats:title>\n            <jats:p>Overall, these results demonstrate that ANXA1 plasma levels are elevated in individuals with type 1 diabetes independent of a significant impairment in renal function. Furthermore, in mouse models with STZ-induced type 1 diabetes, ANXA1 protects against cardiac and renal dysfunction by returning MAPK signalling to baseline and activating pro-survival pathways (Akt). We propose ANXA1 to be a potential therapeutic option for the control of comorbidities in type 1 diabetes.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1007\/s00125-017-4469-y","type":"journal-article","created":{"date-parts":[[2017,10,30]],"date-time":"2017-10-30T13:52:58Z","timestamp":1509371578000},"page":"482-495","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":56,"title":["RETRACTED ARTICLE: Annexin A1 attenuates microvascular complications through restoration of Akt signalling in a murine model of type 1 diabetes"],"prefix":"10.1007","volume":"61","author":[{"given":"Gareth S. 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Please see the Retraction Notice for more detail:","order":6,"name":"change_details","label":"Change Details","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"https:\/\/doi.org\/10.1007\/s00125-025-06418-2","URL":"https:\/\/doi.org\/10.1007\/s00125-025-06418-2","order":7,"name":"change_details","label":"Change Details","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"All data generated or analysed during this study are included in this published article (and its  file).","order":1,"name":"Ethics","group":{"name":"EthicsHeading","label":"Data availability"}},{"value":"We would like to thank the following funding bodies: the British Heart Foundation (Award number: FS\/13\/58\/30648) to GP; the Ministry of Education, Brazil (Grant number: 7326\/2014-09) to RAL; University of Turin (Ricerca Locale Linea B 2015 and Linea A 2016) to MC; the William Harvey Research Foundation to CT; Bart\u2019s and The London Charity Centre of Diabetic Kidney Disease (programme grant: 577\/2348) to MY and CT; and FISM Fondazione Italiana Sclerosi Multipla\u2013Cod. 2014\/R\/21 to ES. We acknowledge support from the National Institute for Health and Research, Biomedical Research Centre award to Guy\u2019s and St Thomas Foundation Trust in partnership with King\u2019s College London.","order":2,"name":"Ethics","group":{"name":"EthicsHeading","label":"Funding"}},{"value":"No conflict of interest declared.","order":3,"name":"Ethics","group":{"name":"EthicsHeading","label":"Duality of interest"}},{"value":"All authors made substantial contributions to conception and design, acquisition of data and interpretation of data; GP, LG, MC, CT and ES drafted the manuscript and provided important intellectual content; all authors reviewed and approved the manuscript. GP, CT and ES are the guarantors of this work.","order":4,"name":"Ethics","group":{"name":"EthicsHeading","label":"Contribution statement"}}]}}