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@ARTICLE{Aich:271329,
      author       = {Aich, Abhishek and Boshnakovska, Angela and Witte, Steffen
                      and Gall, Tanja and Unthan-Fechner, Kerstin and Yousefi,
                      Roya and Chowdhury, Arpita and Dahal, Drishan and Methi,
                      Aditi and Kaufmann, Svenja and Silbern, Ivan and Prochazka,
                      Jan and Nichtova, Zuzana and Palkova, Marcela and
                      Raishbrook, Miles and Koubkova, Gizela and Sedlacek,
                      Radislav and Tröder, Simon E and Zevnik, Branko and Riedel,
                      Dietmar and Michanski, Susann and Möbius, Wiebke and
                      Ströbel, Philipp and Lüchtenborg, Christian and
                      Giavalisco, Patrick and Urlaub, Henning and Fischer, Andre
                      and Brügger, Britta and Jakobs, Stefan and Rehling, Peter},
      title        = {{D}efective mitochondrial {COX}1 translation due to loss of
                      {COX}14 function triggers {ROS}-induced inflammation in
                      mouse liver.},
      journal      = {Nature Communications},
      volume       = {15},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DZNE-2024-01031},
      pages        = {6914},
      year         = {2024},
      abstract     = {Mitochondrial oxidative phosphorylation (OXPHOS) fuels
                      cellular ATP demands. OXPHOS defects lead to severe human
                      disorders with unexplained tissue specific pathologies.
                      Mitochondrial gene expression is essential for OXPHOS
                      biogenesis since core subunits of the complexes are
                      mitochondrial-encoded. COX14 is required for translation of
                      COX1, the central mitochondrial-encoded subunit of complex
                      IV. Here we describe a COX14 mutant mouse corresponding to a
                      patient with complex IV deficiency. COX14M19I mice display
                      broad tissue-specific pathologies. A hallmark phenotype is
                      severe liver inflammation linked to release of mitochondrial
                      RNA into the cytosol sensed by RIG-1 pathway. We find that
                      mitochondrial RNA release is triggered by increased reactive
                      oxygen species production in the deficiency of complex IV.
                      Additionally, we describe a COA3Y72C mouse, affected in an
                      assembly factor that cooperates with COX14 in early COX1
                      biogenesis, which displays a similar yet milder inflammatory
                      phenotype. Our study provides insight into a link between
                      defective mitochondrial gene expression and tissue-specific
                      inflammation.},
      keywords     = {Animals / Reactive Oxygen Species: metabolism / Mice /
                      Liver: metabolism / Liver: pathology / Inflammation:
                      metabolism / Inflammation: genetics / Inflammation:
                      pathology / Electron Transport Complex IV: metabolism /
                      Electron Transport Complex IV: genetics / Oxidative
                      Phosphorylation / Mitochondria: metabolism / Humans / RNA,
                      Mitochondrial: genetics / RNA, Mitochondrial: metabolism /
                      Male / Mitochondrial Proteins: metabolism / Mitochondrial
                      Proteins: genetics / Protein Biosynthesis / Mice, Inbred
                      C57BL / DEAD-box RNA Helicases: metabolism / DEAD-box RNA
                      Helicases: genetics / Female / Mutation / DEAD Box Protein
                      58 / Membrane Proteins / Cyclooxygenase 1 / Reactive Oxygen
                      Species (NLM Chemicals) / Electron Transport Complex IV (NLM
                      Chemicals) / Ddx58 protein, mouse (NLM Chemicals) / RNA,
                      Mitochondrial (NLM Chemicals) / Ptgs1 protein, mouse (NLM
                      Chemicals) / Mitochondrial Proteins (NLM Chemicals) /
                      DEAD-box RNA Helicases (NLM Chemicals) / DEAD Box Protein 58
                      (NLM Chemicals) / Membrane Proteins (NLM Chemicals) /
                      Cyclooxygenase 1 (NLM Chemicals)},
      cin          = {AG Fischer},
      ddc          = {500},
      cid          = {I:(DE-2719)1410002},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC11319346},
      pubmed       = {pmid:39134548},
      doi          = {10.1038/s41467-024-51109-y},
      url          = {https://pub.dzne.de/record/271329},
}