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      TRIM33 prevents pulmonary fibrosis by impairing TGF-β1 signalling.

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          Abstract

          Idiopathic pulmonary fibrosis (IPF) is a devastating disease characterised by myofibroblast proliferation and abnormal extracellular matrix accumulation in the lungs. Transforming growth factor (TGF)-β1 initiates key profibrotic signalling involving the SMAD pathway and the small heat shock protein B5 (HSPB5). Tripartite motif-containing 33 (TRIM33) has been reported to negatively regulate TGF-β/SMAD signalling, but its role in fibrogenesis remains unknown. The objective of this study was to elucidate the role of TRIM33 in IPF.

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          Author and article information

          Journal
          Eur. Respir. J.
          The European respiratory journal
          European Respiratory Society (ERS)
          1399-3003
          0903-1936
          Jun 2020
          : 55
          : 6
          Affiliations
          [1 ] INSERM U1231, Faculty of Medicine and Pharmacy, University of Bourgogne-Franche Comté, Dijon, France.
          [2 ] Division of Pulmonary Sciences and Critical Care Medicine, Dept of Medicine, University of Colorado Denver, Aurora, CO, USA.
          [3 ] Dept of Pulmonary Medicine and Intensive Care Unit, University Hospital, Bourgogne-Franche Comté, Dijon, France.
          [4 ] Reference Center for Rare Lung Diseases, University Hospital, Bourgogne-Franche Comté, Dijon, France.
          [5 ] Cancer Center Georges François Leclerc, Dijon, France.
          [6 ] INSERM U1152, Faculty of Medicine, University of Bichat, Paris, France.
          [7 ] McMaster University, Hamilton, ON, Canada.
          [8 ] These authors codirected this work and contributed equally to this work.
          [9 ] INSERM U1231, Faculty of Medicine and Pharmacy, University of Bourgogne-Franche Comté, Dijon, France philippe.bonniaud@chu-dijon.fr.
          Article
          13993003.01346-2019
          10.1183/13993003.01346-2019
          32184320
          2bdf41ba-3010-4461-926e-e40c622f3ee4
          History

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