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Airway remodeling is an unavoidable pathological characteristic. However, the molecular mechanisms of airway remodeling are incompletely defined.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>lncRNAs highly correlated with transforming growth factor beta 1(TGF\u2013\u03b21) expression were chosen, the lncRNA <jats:italic>ENST00000440406<\/jats:italic> (named HSP90AB1 Assoicated LncRNA 1, <jats:italic>HSALR1<\/jats:italic>) was chosen for further functional experiments. Dual luciferase and ChIP assay were used to detect the upstream of HSALR1, transcriptome sequencing, Cck\u20138, Edu, cell proliferation, cell cycle assay, and WB detection of pathway levels confirmed the effect of HSALR1 on fibroblast proliferation and phosphorylation levels of related pathways. Mice was infected with adeno\u2013associated virus (AAV) to express <jats:italic>HSALR1<\/jats:italic> by intratracheal instillation under anesthesia and was exposure to cigarette smoke, then mouse lung function was performed and the pathological sections of lung tissues were analyzed.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Herein, lncRNA <jats:italic>HSALR1<\/jats:italic> was identified as highly correlated with the TGF\u2013\u03b21 and mainly expressed in human lung fibroblasts. HSALR1 was induced by Smad3 and promoted fibroblasts proliferation. Mechanistically, it could directly bind to HSP90AB1 protein, and acted as a scaffold to stabilize the binding between Akt and HSP90AB1 to promote Akt phosphorylation. In vivo, mice expressed <jats:italic>HSALR1<\/jats:italic> by AAV was exposure to cigarette smoke (CS) for COPD modeling. We found that lung function was worse and airway remodeling was more pronounced in HSLAR1 mice compare to wild type (WT) mice.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Our results suggest that lncRNA <jats:italic>HSALR1<\/jats:italic> binds to HSP90AB1 and Akt complex component, and enhances activity of the TGF\u2013\u03b21 smad3\u2013independent pathway. This finding described here suggest that lncRNA can participate in COPD development, and <jats:italic>HSLAR1<\/jats:italic> is a promising molecular target of COPD therapy.<\/jats:p><\/jats:sec>","DOI":"10.1002\/ctm2.1292","type":"journal-article","created":{"date-parts":[[2023,6,15]],"date-time":"2023-06-15T05:34:50Z","timestamp":1686807290000},"source":"Crossref","is-referenced-by-count":15,"title":["Smad3\u2010mediated lncRNA <i>HSALR1<\/i> enhances the non\u2010classic signalling pathway of TGF\u2010\u03b21 in human bronchial fibroblasts by binding to HSP90AB1"],"prefix":"10.1002","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1018-6641","authenticated-orcid":false,"given":"Erkang","family":"Yi","sequence":"first","affiliation":[{"name":"Guangzhou Institute of Respiratory Health &amp; State Key Laboratory of Respiratory Disease &amp; National Clinical Research Center for Respiratory Disease &amp; National Center for Respiratory Medicine The First Affiliated Hospital of Guangzhou Medical University  Guangzhou Guangdong China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Biting","family":"Lin","sequence":"additional","affiliation":[{"name":"GMU\u2010GIBH Joint School of Life Sciences Guangzhou Medical University  Guangzhou Guangdong China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yi","family":"Zhang","sequence":"additional","affiliation":[{"name":"GMU\u2010GIBH Joint School of Life Sciences Guangzhou Medical University  Guangzhou Guangdong China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaoyu","family":"Wang","sequence":"additional","affiliation":[{"name":"Guangzhou Institute of Respiratory Health &amp; 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