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Here, we demonstrate a crucial role of WNT5A\/JNK\/ROCK signaling that rapidly coordinates the activation of latent TGF-\u03b2 in fibrotic diseases. WNT5A was identified as a predominant noncanonical WNT ligand in fibrotic diseases such as systemic sclerosis, sclerodermatous chronic graft-versus-host disease, and idiopathic pulmonary fibrosis, stimulating fibroblast-to-myofibroblast transition and tissue fibrosis by activation of latent TGF-\u03b2. The activation of latent TGF-\u03b2 requires rapid JNK- and ROCK-dependent cytoskeletal rearrangements and integrin \u03b1\n                    <jats:sub>V<\/jats:sub>\n                    (ITGAV). Conditional ablation of WNT5A or its downstream targets prevented activation of latent TGF-\u03b2, rebalanced TGF-\u03b2 signaling, and ameliorated experimental fibrosis. We thus uncovered what we believe to be a novel mechanism for the aberrant activation of latent TGF-\u03b2 in fibrotic diseases and provided evidence for targeting WNT5A\/JNK\/ROCK signaling in fibrotic diseases as a new therapeutic approach.\n                  <\/jats:p>","DOI":"10.1172\/jci159884","type":"journal-article","created":{"date-parts":[[2024,5,14]],"date-time":"2024-05-14T14:00:32Z","timestamp":1715695232000},"source":"Crossref","is-referenced-by-count":71,"title":["Noncanonical WNT5A controls the activation of latent TGF-\u03b2 to drive fibroblast activation and tissue fibrosis"],"prefix":"10.1172","volume":"134","author":[{"given":"Thuong","family":"Trinh-Minh","sequence":"first","affiliation":[{"name":"Department of Rheumatology and"},{"name":"Hiller Research Center, University Hospital D\u00fcsseldorf, Medical Faculty of Heinrich Heine University, D\u00fcsseldorf, North-Rhine-Westphalia, 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