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Our study focused on the role of O-GlcNAcylation of Yes-associated protein 1 (YAP1) in exacerbating this injury by regulating autophagy and mitochondrial autophagy pathways. We found that hypoxia-reoxygenation robustly activated the Hippo-YAP1 signaling pathway, leading to increased damage in lung epithelial cells. Concurrently, autophagy and mitochondrial autophagy levels were significantly upregulated, indicating cellular stress responses. During actual lung transplantation, ischemia-reperfusion resulted in a marked increase in autophagy and mitochondrial autophagy levels, accompanied by elevated tissue damage. Notably, YAP1 played a crucial role in orchestrating these processes, as its knockdown reduced autophagy and mitochondrial autophagy levels under both hypoxia-reoxygenation and ischemia-reperfusion conditions. We further elucidated that OGT-mediated O-GlcNAc modification of YAP1 enhanced its interaction with HIF1\u03b1, activating downstream hypoxia-responsive molecules. Knockdown of the key enzyme OGT significantly mitigated autophagy, mitophagy, and associated damage in lung epithelial cells and transplant tissues subjected to hypoxia-reoxygenation and ischemia-reperfusion. These findings reveal the intricate interplay between O-GlcNAcylation of YAP1, HIF1\u03b1 binding, autophagy activation, and mitochondrial autophagy in driving lung transplant ischemia-reperfusion injury, suggesting potential therapeutic targets for ameliorating its detrimental effects.<\/jats:p>","DOI":"10.1038\/s41419-026-08548-w","type":"journal-article","created":{"date-parts":[[2026,3,15]],"date-time":"2026-03-15T04:53:35Z","timestamp":1773550415000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["O-GlcNAcylation of YAP1 promotes lung transplant ischemia-reperfusion injury via binding to HIF1\u03b1 transcription factor and activating autophagy and mitophagy"],"prefix":"10.1038","volume":"17","author":[{"given":"Shaohua","family":"Dai","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xuemei","family":"Wan","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lingchun","family":"Xia","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lei","family":"Xu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Chunfan","family":"Xie","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Guohui","family":"Wang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0009-0000-1438-9449","authenticated-orcid":false,"given":"Jian","family":"Tang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2026,3,15]]},"reference":[{"key":"8548_CR1","doi-asserted-by":"publisher","first-page":"1333.","DOI":"10.3390\/cells10061333","volume":"10","author":"TF Chen-Yoshikawa","year":"2021","unstructured":"Chen-Yoshikawa TF. 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