{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,15]],"date-time":"2026-09-15T07:07:19Z","timestamp":1789456039368,"version":"build-2803163510"},"reference-count":41,"publisher":"Wiley","issue":"17","license":[{"start":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T00:00:00Z","timestamp":1788912000000},"content-version":"vor","delay-in-days":8,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T00:00:00Z","timestamp":1788220800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2026,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Idiopathic pulmonary fibrosis (IPF) is a lethal lung disorder that is associated with aberrant lipid metabolism. N6\u2010methyladenosine (m6A) methylation is involved in IPF progression. However, whether METTL3, a m6A methyltransferase, modulates lipid metabolism in IPF remains unknown. In this study, we aimed to investigate the effects of METTL3 on fibrosis and lipid accumulation and identify the molecular mechanism. PF mouse model was generated by bleomycin. WI\u201038 cells were stimulated with TGF\u2010\u03b21 to mimic the IPF\u2010caused damage. Lipids were observed using Nile Red staining and marker detection. Fibrosis was evaluated using Masson's Trichrome staining and marker detection. The molecular mechanism was analysed by methylated RNA immunoprecipitation and dual\u2010luciferase reporter assay. We found that METTL3 is highly expressed in IPF mice and TGF\u2010\u03b21\u2010induced WI\u201038 cells. Knockdown of METTL3 inhibited lipid accumulation and fibrosis In\u00a0Vitro and In\u00a0Vivo. Additionally, interference with METTL3 suppressed the m6A methylation of PLIN2, enhanced its stability, and increased its expression. Knockdown of PLIN2 reversed the inhibition of lipid accumulation and fibrosis caused by METTL3 silence. In conclusion, interfering with METTL3 attenuates IPF progression by suppressing lipid deposition, which is associated with the increased stability of PLIN2 suggesting a promising therapeutic target for IPF.<\/jats:p>","DOI":"10.1111\/jcmm.71239","type":"journal-article","created":{"date-parts":[[2026,9,10]],"date-time":"2026-09-10T05:20:38Z","timestamp":1789017638000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["<scp>METTL3<\/scp>\n                    Promotes Lipid Deposition and Pulmonary Fibrosis by Destabilizing\n                    <scp>PLIN2<\/scp>\n                    in a m6A\u2010Dependent Manner"],"prefix":"10.1111","volume":"30","author":[{"given":"Qiping","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Respiratory and Critical Care Medicine Second Affiliated Hospital of Chongqing Medical University  Chongqing 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