{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,13]],"date-time":"2026-04-13T19:58:52Z","timestamp":1776110332798,"version":"3.50.1"},"reference-count":32,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2024,12,25]],"date-time":"2024-12-25T00:00:00Z","timestamp":1735084800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Wound Repair Regeneration"],"published-print":{"date-parts":[[2025,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Foot ulcers are amongst the most prevalent complications of diabetes, known for their delayed healing process. Recent research indicates that the transcription factor forkhead box M1 (FOXM1) plays a role in promoting diabetic ulcer repair. However, the precise mechanisms underlying FOXM1 functions in this context remain unclear. This study aimed to clarify the role of tripartite motif\u2010containing protein 72 (TRIM72)\u2010mediated endoplasmic reticulum stress in FOXM1 promotive effects. Immunohistochemistry revealed that FOXM1 expression was significantly reduced in the lesion tissues of diabetic foot ulcer patients. In vitro experiments revealed a decrease in FOXM1 expression in cultured dermal fibroblasts under high glucose conditions. Activating FOXM1 with a plasmid accelerated the proliferation, migration, and differentiation of dermal fibroblasts and mitigated endoplasmic reticulum stress under high glucose conditions. Additionally, ChIP and luciferase reporter gene assays confirmed that FOXM1 suppressed TRIM72 expression transcriptionally by binding to its promoter. Furthermore, high glucose induced ubiquitination of adenosine 5\u2032\u2010monophosphate\u2010activated protein kinase alpha (AMPK\u03b1), whilst inactivation of AMPK\u03b1 signalling reversed the aforementioned effects of FOXM1 on cells. Finally, the FOXM1\u2010overexpressing plasmid was transfected in vivo, which promoted wound healing in a murine diabetic ulcer model. In conclusion, FOXM1 reduces endoplasmic reticulum stress by inhibiting TRIM72\u2010mediated AMPK\u03b1 ubiquitination, thereby accelerating the healing of diabetic ulcers.<\/jats:p>","DOI":"10.1111\/wrr.13247","type":"journal-article","created":{"date-parts":[[2024,12,26]],"date-time":"2024-12-26T03:21:06Z","timestamp":1735183266000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Suppression of <scp>TRIM72<\/scp>\u2010mediated endoplasmic reticulum stress facilitates <scp>FOXM1<\/scp> promotion of diabetic ulcer healing"],"prefix":"10.1111","volume":"33","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5717-5325","authenticated-orcid":false,"given":"Lingling","family":"Peng","sequence":"first","affiliation":[{"name":"Department of Dermatology The Second Affiliated Hospital of Xi'an Jiaotong University  Xi'an 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