{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,28]],"date-time":"2026-07-28T14:09:56Z","timestamp":1785247796894,"version":"3.55.0"},"reference-count":36,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2022,11,27]],"date-time":"2022-11-27T00:00:00Z","timestamp":1669507200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82271678"],"award-info":[{"award-number":["82271678"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003392","name":"Natural Science Foundation of Fujian Province","doi-asserted-by":"publisher","award":["2021J011347"],"award-info":[{"award-number":["2021J011347"]}],"id":[{"id":"10.13039\/501100003392","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["American J Rep Immunol"],"published-print":{"date-parts":[[2023,3]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Endometriosis is a benign gynecological disease with the feature of estrogen dependence and inflammation. The function of autophagy and the correlation with inflammation were not yet revealed.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Autophagosomes were detected by transmission electron microscopy. Gene Expression Omnibus (GEO) database was referred to analyze the expression of autophagy\u2010related genes. Quantification of mRNA and protein expression was examined by qRT\u2010PCR and Western Blot. Immunohistochemistry was performed to explore the expression of proteins in tissues. The mouse model of endometriosis was performed to analyze the autophagic activity and effect of LXA4.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The expression of autophagy\u2010related genes in endometriotic lesions were unusually changed. The number of autophagosomes and LC3B\u2010II expression was diminished, and p62 was increased in ectopic lesions from both patients and mice. Interleukin 1\u03b2 (IL1\u03b2) attenuated the expression of LC3B and promoted the level p62. The autophagy activator MG\u2010132 upregulated the expression of LC3B and reduced IL1\u03b2, IL6, and p62. LXA4 reversed the inhibitory effect of IL1\u03b2 on the expression of LC3B and p62, and blocking the receptor of LXA4 AhR (aryl hydrocarbon receptor) resulted in the incapacitation of LXA4 to influence the effect of IL1\u03b2. LXA4 depressed the phosphorylation of AKT and mTOR to against IL1\u03b2, and blocking AhR negatively regulated the effect of LXA4 on AKT\/mTOR pathway. LXA4 reduced the ectopic lesions and the expression of IL1\u03b2 and p62, but enhanced LC3B\u2010II in endometriotic mouse models.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>In endometriosis, increased inflammation of ectopic lesions prominently depresses autophagy. LXA4 could regulate autophagy by suppressing inflammatory response through AhR\/AKT\/mTOR pathway.<\/jats:p><\/jats:sec>","DOI":"10.1111\/aji.13659","type":"journal-article","created":{"date-parts":[[2022,11,22]],"date-time":"2022-11-22T08:04:19Z","timestamp":1669104259000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Lipoxin A4 depresses inflammation and promotes autophagy via AhR\/mTOR\/AKT pathway to suppress endometriosis"],"prefix":"10.1111","volume":"89","author":[{"given":"Zhi\u2010Xiong","family":"Huang","sequence":"first","affiliation":[{"name":"Clinical Medical Research Center for Obstetrics and Gynecology Diseases of Fujian Province Laboratory of Research and Diagnosis of Gynecological Diseases of Xiamen City Department of Obstetrics and Gynecology The First Affiliated Hospital of Xiamen University School of Medicine, Xiamen University  Xiamen 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