{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T09:44:11Z","timestamp":1792057451901,"version":"4.4.0"},"reference-count":48,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T00:00:00Z","timestamp":1792022400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T00:00:00Z","timestamp":1792022400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82470065"],"award-info":[{"award-number":["82470065"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82270077"],"award-info":[{"award-number":["82270077"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["MedComm"],"published-print":{"date-parts":[[2026,11]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal interstitial lung disease characterized by excessive extracellular matrix (ECM) deposition and elevated tissue stiffness. While aberrant mechanotransduction is increasingly recognized as a key driver of fibrotic progression, the mechanisms by which mechanical cues orchestrate macrophage dysfunction remain poorly elucidated. Here, we identify the mechanosensitive ion channel PIEZO1 as a key mediator coupling matrix stiffening to macrophage inflammatory activation in pulmonary fibrosis. We demonstrate that PIEZO1 is substantially upregulated in fibrotic lungs, and that its activation drives intracellular calcium overload via the CISD1\/IP3R signaling axis. This process elicits aberrant opening of the mitochondrial permeability transition pore (MPTP), causing mitochondrial dysfunction and augmented pro\u2010inflammatory macrophage polarization. Conversely, PIEZO1 inhibition suppresses the CISD1\/IP3R signaling cascade, alleviates calcium dysregulation, prevents mitochondrial damage, and attenuates inflammatory activation. In vitro CISD1 inhibition ameliorates PIEZO1\u2010driven mitochondrial abnormalities and pro\u2010inflammatory signaling in macrophages. Furthermore, genetic knockdown of CISD1 mitigates mitochondrial abnormalities and attenuates bleomycin (BLM)\u2010induced lung fibrosis in mice. Collectively, these findings identify a previously unrecognized PIEZO1\/CISD1\/IP3R mechanotransduction axis coupling tissue stiffening to macrophage\u2010mediated inflammation and fibrosis. This study offers mechanistic insights into fibrosis\u2010associated immune dysregulation, highlighting PIEZO1 and CISD1 as promising therapeutic targets for pulmonary fibrosis.<\/jats:p>","DOI":"10.1002\/mco2.71080","type":"journal-article","created":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T08:46:00Z","timestamp":1792053960000},"source":"Crossref","is-referenced-by-count":0,"title":["The PIEZO1\/CISD1\/IP3R Mechanotransduction Axis Drives Macrophage Mitochondrial Dysfunction and Inflammatory Activation in Pulmonary Fibrosis"],"prefix":"10.1002","volume":"7","author":[{"ORCID":"https:\/\/orcid.org\/0009-0009-2418-9761","authenticated-orcid":false,"given":"Yungeng","family":"Wei","sequence":"first","affiliation":[{"name":"State Key Laboratory of Respiratory Disease National Clinical Research Center for Respiratory Disease National Center for Respiratory Medicine Guangzhou Institute of Respiratory Health The First Affiliated Hospital of Guangzhou Medical University  Guangzhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chao","family":"Xie","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Respiratory Disease National Clinical Research Center for Respiratory Disease National Center for Respiratory Medicine Guangzhou Institute of Respiratory Health The First Affiliated Hospital of Guangzhou Medical University  Guangzhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiangsheng","family":"Yang","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Respiratory Disease National Clinical Research Center for Respiratory Disease National Center for Respiratory Medicine Guangzhou Institute of Respiratory Health The First Affiliated Hospital of Guangzhou Medical University  Guangzhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3383-0989","authenticated-orcid":false,"given":"Xiao Xiao","family":"Tang","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Respiratory Disease National Clinical Research Center for Respiratory Disease National Center for Respiratory Medicine Guangzhou Institute of Respiratory Health The First Affiliated Hospital of Guangzhou Medical University  Guangzhou China"},{"name":"Guangzhou National Laboratory  Guangzhou China"},{"name":"GMU\u2010GIBH Joint School of Life Sciences Guangzhou Medical University  Guangzhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,10,15]]},"reference":[{"issue":"1","key":"e_1_2_12_2_1","doi-asserted-by":"crossref","first-page":"306","DOI":"10.1038\/s41392-024-02011-y","article-title":"Overexpression of STX11 Alleviates Pulmonary Fibrosis by Inhibiting Fibroblast Activation via the PI3K\/AKT\/mTOR Pathway","volume":"9","author":"Huang G.","year":"2024","journal-title":"Signal Transduction and Targeted Therapy"},{"key":"e_1_2_12_3_1","doi-asserted-by":"crossref","DOI":"10.1016\/j.bbadis.2025.167992","article-title":"Impaired Ciliogenesis in Small Airway Epithelial Cells Involves in the Development of Idiopathic Pulmonary Fibrosis","volume":"1871","author":"Wang Z.","year":"2025","journal-title":"Biochimica et Biophysica Acta (BBA)\u2014Molecular Basis of Disease"},{"issue":"1","key":"e_1_2_12_4_1","doi-asserted-by":"crossref","first-page":"118","DOI":"10.1186\/s12931-023-02424-3","article-title":"Elevated Expression of Macrophage MERTK Exhibits Profibrotic Effects and Results in Defective Regulation of Efferocytosis Function in Pulmonary Fibrosis","volume":"24","author":"She Y.","year":"2023","journal-title":"Respiratory Research"},{"issue":"148","key":"e_1_2_12_5_1","doi-asserted-by":"crossref","DOI":"10.1183\/16000617.0033-2018","article-title":"Matrix Abnormalities in Pulmonary Fibrosis","volume":"27","author":"Upagupta C.","year":"2018","journal-title":"European Respiratory Review"},{"issue":"6","key":"e_1_2_12_6_1","doi-asserted-by":"crossref","first-page":"1311","DOI":"10.1083\/jcb.200704042","article-title":"Myofibroblast Contraction Activates Latent TGF\u2010beta1 From the Extracellular Matrix","volume":"179","author":"Wipff P. 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