TOM5 regulates the mitochondrial membrane potential of alveolar epithelial cells in organizing pneumonia.

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  • Additional Information
    • Source:
      Publisher: Taylor & Francis Country of Publication: England NLM ID: 9511366 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1743-2928 (Electronic) Linking ISSN: 13510002 NLM ISO Abbreviation: Redox Rep Subsets: MEDLINE
    • Publication Information:
      Publication: 2016- : Abingdon : Taylor & Francis
      Original Publication: Edinburgh ; New York : Churchill Livingstone, c1994-
    • Subject Terms:
      Alveolar Epithelial Cells*/metabolism ; Alveolar Epithelial Cells*/pathology ; Membrane Potential, Mitochondrial*/physiology; Animals ; Mice ; Humans ; Mitochondrial Precursor Protein Import Complex Proteins ; Male ; Apoptosis ; Female ; Cell Proliferation ; Mice, Inbred C57BL ; Disease Models, Animal ; Cryptogenic Organizing Pneumonia/pathology ; Cryptogenic Organizing Pneumonia/metabolism ; Organizing Pneumonia
    • Abstract:
      Deficiency of TOM5, a mitochondrial protein, causes organizing pneumonia (OP) in mice. The clinical significance and mechanisms of TOM5 in the pathogenesis of OP remain elusive. We demonstrated that TOM5 was significantly increased in the lung tissues of OP patients, which was positively correlated with the collagen deposition. In a bleomycin-induced murine model of chronic OP, increased TOM5 was in line with lung fibrosis. In vitro, TOM5 regulated the mitochondrial membrane potential in alveolar epithelial cells. TOM5 reduced the proportion of early apoptotic cells and promoted cell proliferation. Our study shed light on the roles of TOM5 in OP.
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    • Contributed Indexing:
      Keywords: Organizing pneumonia; TOM5; alveolar epithelial cells; mitochondrial membrane potential; bleomycin
    • Accession Number:
      0 (Mitochondrial Precursor Protein Import Complex Proteins)
    • Publication Date:
      Date Created: 20240525 Date Completed: 20240525 Latest Revision: 20240531
    • Publication Date:
      20240531
    • Accession Number:
      PMC11134018
    • Accession Number:
      10.1080/13510002.2024.2354625
    • Accession Number:
      38794801