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This study demonstrates that methyltransferase\u2010like 1 (METTL1), an m7G methyltransferase, is significantly upregulated in epidermal keratinocytes of human psoriatic lesions and imiquimod (IMQ)\u2010induced murine models. Utilizing mice with an inducible keratinocyte\u2010specific\n                    <jats:italic>Mettl1<\/jats:italic>\n                    deletion (\n                    <jats:italic>Mettl1<\/jats:italic>\n                    <jats:sup>fl\/fl<\/jats:sup>\n                    <jats:italic>Krt14<\/jats:italic>\n                    \u2010Cre\n                    <jats:sup>ERT2<\/jats:sup>\n                    ), the research reveals significantly attenuated psoriasiform inflammation and decreased neutrophil infiltration relative to\n                    <jats:italic>Mettl1<\/jats:italic>\n                    <jats:sup>fl\/fl<\/jats:sup>\n                    counterparts. Mechanistically, METTL1 drives inflammation by augmenting\n                    <jats:italic>Bdkrb1<\/jats:italic>\n                    mRNA stability through m7G modification. This stabilization leads to elevated bradykinin receptor B1 (BDKRB1) protein expression, which activates the p38 mitogen\u2010activated protein kinase (MAPK) pathway in keratinocytes, promoting the secretion of key proinflammatory C\u2010X\u2010C motif chemokine ligand (CXCL) chemokines and robust neutrophil chemotaxis. Crucially, both in vivo genetic BDKRB1 overexpression and pharmacological BDKRB1 activation successfully rescue the attenuated inflammatory phenotype in\n                    <jats:italic>Mettl1<\/jats:italic>\n                    \u2010deficient mice, firmly validating this specific signaling cascade. Conversely, pharmacological inhibition of the METTL1\u2013BDKRB1 axis effectively mitigates psoriasiform inflammation. Collectively, these data establish that METTL1 modulates psoriasis by fostering p38\u2010dependent chemokine production and neutrophil recruitment, identifying the METTL1\u2013BDKRB1 axis as a novel therapeutic target.\n                  <\/jats:p>","DOI":"10.1002\/advs.75970","type":"journal-article","created":{"date-parts":[[2026,6,9]],"date-time":"2026-06-09T10:56:41Z","timestamp":1781002601000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Epidermal METTL1\u2010Mediated m7G Modification Drives Psoriatic Inflammation by Stabilizing\n                    <i>Bdkrb1<\/i>\n                    and Orchestrating Neutrophil Recruitment"],"prefix":"10.1002","volume":"13","author":[{"given":"Chang","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Dermatology the First Affiliated Hospital of Anhui Medical University  Hefei China"},{"name":"Institute of Dermatology Anhui Medical University  Hefei 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