{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T01:18:08Z","timestamp":1790039888715,"version":"4.0.1"},"reference-count":35,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2024,10,31]],"date-time":"2024-10-31T00:00:00Z","timestamp":1730332800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Experimental Physiology"],"published-print":{"date-parts":[[2024,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Intestinal ischaemia\u2013reperfusion (I\/R) is a common clinical pathology with high incidence and mortality rates. However, the mechanisms underlying intestinal I\/R injury remain unclear. In this study, we investigated the role and mechanism of chitinase 3\u2010like 1 (CHI3L1) during intestinal I\/R injury. Therefore, we analysed the expression levels of CHI3L1 in the intestinal tissue of an intestinal I\/R rat model and explored its effects and mechanism in a hypoxia\u2013reoxygenation (H\/R) IEC\u20106 cell model. We found that intestinal I\/R injury elevated CHI3L1 levels in the serum, ileum and duodenum, whereas H\/R enhanced CHI3L1 expression in IEC\u20106 cells. The H\/R\u2010induced inhibition of proliferation and apoptosis was alleviated by CHI3L1 knockdown and aggravated by CHI3L1 overexpression. In addition, CHI3L1 knockdown alleviated, and CHI3L1 overexpression aggravated, the H\/R\u2010induced inflammatory response and oxidative stress. Mechanistically, CHI3L1 overexpression weakened the activation of the phosphoinositide 3\u2010kinase (PI3K)\/AKT pathway, suppressed the nuclear translocation of Nrf2, and promoted the nuclear translocation of nuclear factor \u03baB (NF\u2010\u03baB). Moreover, CHI3L1 knockdown had the opposite effect on the PI3K\/AKT pathway, Nrf2, and NF\u2010\u03baB. Moreover, the PI3K inhibitor LY294002 blocked the effect of CHI3L1 knockdown on the H\/R\u2010induced inhibition of proliferation, apoptosis, inflammatory response and oxidative stress. In conclusion, CHI3L1 expression was induced during intestinal I\/R and H\/R injury in IEC\u20106 cells, and CHI3L1 overexpression aggravated H\/R injury in IEC\u20106 cells by inhibiting the PI3K\/AKT signalling pathway. Therefore, CHI3L1 may be an effective target for controlling intestinal I\/R injury.<\/jats:p>","DOI":"10.1113\/ep091768","type":"journal-article","created":{"date-parts":[[2024,10,31]],"date-time":"2024-10-31T16:40:16Z","timestamp":1730392816000},"page":"2073-2087","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Chitinase 3\u2010like 1 overexpression aggravates hypoxia\u2013reoxygenation injury in IEC\u20106 cells by inhibiting the PI3K\/AKT signalling pathway"],"prefix":"10.1113","volume":"109","author":[{"given":"Lei","family":"Mi","sequence":"first","affiliation":[{"name":"Department of Gastrointestinal Surgery The Affiliated Taian City Central Hospital of Qingdao University  Tai'an China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jie","family":"Jin","sequence":"additional","affiliation":[{"name":"Department of Traditional Chinese Medicine The Affiliated Taian City Central Hospital of 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