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Here, we tested the role of N6-methyladenosine (m6A) modification of\n            <jats:italic>forkhead box protein O1<\/jats:italic>\n            (\n            <jats:italic>Foxo1<\/jats:italic>\n            ) mRNA in lung regeneration after pneumonectomy (PNX) in mice, a model for lung regrowth after surgical resection. Endothelial cell (EC)\u2013specific knockout of\n            <jats:italic>methyltransferase-like 3<\/jats:italic>\n            (\n            <jats:italic>Mettl3<\/jats:italic>\n            ) and\n            <jats:italic>Foxo1<\/jats:italic>\n            caused nonproductive intussusceptive angiogenesis (IA), which impaired regeneration and enhanced fibrosis. This nonproductive IA was characterized by enhanced endothelial proliferation and increased vascular splitting with increased numbers of pillar ECs. Endothelial-selective knockout of\n            <jats:italic>Mettl3<\/jats:italic>\n            in mice stimulated nonproductive IA and up-regulation of profibrotic factors after PNX, promoting regeneration to fibrotic transition. EC-specific mutation of m6A modification sites in the\n            <jats:italic>Foxo1<\/jats:italic>\n            gene in mice revealed that endothelial\n            <jats:italic>Mettl3<\/jats:italic>\n            modified A504 and A2035 sites in the\n            <jats:italic>Foxo1<\/jats:italic>\n            mRNA to maintain pro-regenerative endothelial glycolysis, ensuring productive IA and lung regeneration without fibrosis. Suppression of\n            <jats:italic>Mettl3-Foxo1<\/jats:italic>\n            signaling stimulated a subset of hyperglycolytic and hyperproliferative\n            <jats:italic>6-phosphofructo-2-kinase\/fructose-2<\/jats:italic>\n            ,\n            <jats:italic>6-biphosphatase 3<\/jats:italic>\n            (\n            <jats:italic>Pfkfb3<\/jats:italic>\n            )\n            <jats:sup>+<\/jats:sup>\n            ,\n            <jats:italic>Ras homolog family member J<\/jats:italic>\n            (\n            <jats:italic>Rhoj<\/jats:italic>\n            )\n            <jats:sup>+<\/jats:sup>\n            , and\n            <jats:italic>platelet-derived growth factor subunit B<\/jats:italic>\n            (\n            <jats:italic>Pdgfb<\/jats:italic>\n            )\n            <jats:sup>+<\/jats:sup>\n            ECs in both human and mouse lungs with fibrosis. Inhibiting this\n            <jats:italic>Pfkfb3<\/jats:italic>\n            <jats:sup>+<\/jats:sup>\n            <jats:italic>Rhoj<\/jats:italic>\n            <jats:sup>+<\/jats:sup>\n            <jats:italic>Pdgfb<\/jats:italic>\n            <jats:sup>+<\/jats:sup>\n            EC subset normalized IA, alleviated fibrosis, and restored regeneration in bleomycin (BLM)\u2013injured mouse lungs. We found that m6A modification of\n            <jats:italic>Foxo1<\/jats:italic>\n            in the mouse vasculature promoted lung regeneration over fibrosis after PNX and BLM injury.\n          <\/jats:p>","DOI":"10.1126\/scitranslmed.ado5266","type":"journal-article","created":{"date-parts":[[2024,8,28]],"date-time":"2024-08-28T18:01:14Z","timestamp":1724868074000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":23,"title":["Inhibiting endothelial\n            <i>Rhoj<\/i>\n            blocks profibrotic vascular intussusception and angiocrine factors to sustain lung regeneration"],"prefix":"10.1126","volume":"16","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3746-4381","authenticated-orcid":true,"given":"Jie","family":"Ma","sequence":"first","affiliation":[{"name":"Key Lab of Birth Defects and Related Diseases of Women and Children of MOE; State Key Lab of Biotherapy; State Key Laboratory of Respiratory Health and Multimorbidity; NHC Key Laboratory of Chronobiology; Sichuan-Chongqing Key Lab of Bio-Resource Research and Utilization; Development and Related Diseases of Women and Children Key Lab of Sichuan Province; West China Second University Hospital, College of Life Sciences, Sichuan University, Chengdu 610041, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0009-0220-6348","authenticated-orcid":true,"given":"Liyin","family":"Zhang","sequence":"additional","affiliation":[{"name":"Key Lab of Birth Defects and Related Diseases of Women and Children of MOE; State Key Lab of Biotherapy; State Key Laboratory of Respiratory Health and Multimorbidity; NHC Key Laboratory of Chronobiology; Sichuan-Chongqing Key Lab of Bio-Resource Research and Utilization; Development and Related Diseases of Women and Children Key Lab of Sichuan Province; West China Second University Hospital, College of Life Sciences, Sichuan University, Chengdu 610041, 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